Tuesday, May 8, 2012

Dementia Treatments -In Traditional Chinese Medicine Perspective

I. Dementia
About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. Dementia is the loss of mental ability that is severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people. American typical diet contains high amount of saturated and trans fat, artificial ingredients with less fruits and vegetable which can lead to dementia and other kind of diseases.

II. Treatments
C. In traditional Chinese Medicine Perspective(1)
In the study to evaluate the effect of TCM in dementia at the Unilever R&D Shanghai, and Unilever R&D Vlaardingen, Dr. and the team of researchers indicated that Traditional Chinese Medicine (TCM) has a 3000 years' history of human use. A literature survey addressing traditional evidence from human studies was done, with key result that top 10 TCM herb ingredients including Poria cocos, Radix polygalae, Radix glycyrrhizae, Radix angelica sinensis, and Radix rehmanniae were prioritized for highest potential benefit to dementia intervention, related to the highest frequency of use in 236 formulae collected from 29 ancient Pharmacopoeias, ancient formula books, or historical archives on ancient renowned TCM doctors, over the past 10 centuries. Based on the history of use, there was strong clinical support that Radix polygalae is memory improving. Pharmacological investigation also indicated that all the five ingredients mentioned above can elicit memory-improving effects in vivo and in vitro via multiple mechanisms of action. And according to Ancient Records on TCM for Cognitive Decline. The scientists wrote that dementia is as a result of
1. Deficiency of Energy, mainly from the kidney, heart, and spleen, especially from the kidney.
Deficiency of energy is similar to “Qi” deficiency in TCM. According TCM lore Qi is the essential substance that makes up the body and maintains various physiological activities, similar to flow of energy in the body. The energy is mainly from the kidney, heart, and spleen, especially from the kidney.  In TCM, the energy from the kidney is called kidney essence which can produce marrow including cerebral marrow, spinal cord, and bone marrow. The cerebral marrow can nourish the brain and maintain the physiological functions of the brain. If the kidney essence is insufficient, the production of cerebral marrow will be reduced, leading to various symptoms, such as headache, dizziness, amnesia, and retard response.

2.  Blood Stasis
Normally the blood is pumped by the heart to flow in the vessels. If blood circulation is stagnated or slowed down by certain factors such as cold, emotional disorder, aging, consumptive disease, and overstrain, it will result in retention of blood flow in the vessels or organs, a pathological condition named blood stasis. The cognitive function will decline, due to long-term global hypo-perfusion in cerebral blood flow or acute focal stroke in memory-related cerebral parenchyma.

3.  Toxins
As the function of internal organs in the elderly decline, the balance between host defense and external toxins in the body is disrupted. Pathological or physiological products occur and form toxin including waste of “water” and “endogenous fire”, which result from the poor digestion, accumulates into phlegm and retention of fluid, and caused by mental disorder, attack from pathological factors, and imbalance within the body, respectively. If such toxins can not be eliminated quickly the blood circulation and mental acuity will be affected, eventually contributing to the onset of dementia.

Finally, the authors summarized "in TCM philosophy, AD is assumed to be induced by kidney essence vacuity and toxin (turbid phlegm).  The amnestic mild cognitive impairment in elderly population has been disclosed in a clinical investigation to correlate with kidney essence vacuity and turbid phlegm blocking upper orifices. The whole cognitive function may worsen because of the aggravation of kidney essence vacuity, deficiency of blood and qi, phlegm and heat toxin and may eventually lead to multiple cognitive domains impairment, even dementia"

Further to the article, the authors also indicated that Catalpol, an iridoid glycoside, isolated from the fresh Radix rehmanniae and existed broadly in many plants all over the world has many biological functions such as anti-inflammation, promoting of sex hormones production, protection of liver damage, and reduction of elevated blood sugar.  
Recently, catalpol has been identified as a vital active with robust cognitive potential (Figure 4). Behaviour studies exhibited that catalpol reversed brain damage and memory deficits in mice induced by lipopolysaccharide (LPS) and D-galactose and in gerbils by cerebral ischemia. The nootropic and neuroprotective efficacy of catalpol probably resulted from a variety of underlying molecular mechanisms (Table 7).
(i)Antioxidant activity: catalpol promoted endogenous antioxidant enzyme activities,  superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and antioxidant glutathione (GSH), cut down malondialdehyde (MDA) and reactive oxygen species (ROS) generation in PC12 cells and astrocytes primary cultures, exposed to oxygen and glucose deprivation  or H2O2, and in senescent mice induced by D-galactose [79–81, 86, 89, 91, 92].

(ii)Anti-inflammatory activity: catalpol significantly reduced the release of ROS, TNF-α, nitric oxide (NO) and inducible nitric oxide synthase (iNOS) expression after Aβ (1–42)-induced microglial activation in primary cortical neuron-glia cultures, and LPS-induced nuclear factor-kappa B (NF-κB) activation in mice [78, 87].

(iii)Neurogenetic activity: catalpol can enhance axonal growth of cortical neurons cultured in vitro from 24 h newly born rat, at 1–5 mg/mL and ameliorate age-related presynaptic proteins decline (synaptophysin and GAP-43), and neuroplasticity loss in the hippocampus of the aged rats, by upregulating protein kinase C (PKC) and brain-derived neurotrophic factor (BDNF) [85, 88].

 (iv)Antiapoptotic activity: catalpol not only suppressed the downregulation of Bcl-2, upregulation of Bax, and the release of mitochondrial cytochrome c to cytosol, but also attenuated caspase-3 activation, poly-ADP-ribose polymerase (PARP) cleavage, and eventually protected against H2O2-induced apoptosis in PC12 cells and in the ischemic dorsal hippocampus of gerbils subject to CCAO [82–84, 90]. (v)In addition, the function to stimulate the production of adrenal cortical hormones, which increases the production of sex hormones, is likely implicated into the cognitive benefit of catalpol in menopausal women [92]. 



Sources
(1) http://www.hindawi.com/journals/ecam/2012/692621/


Dementia Treatments of Alzheimer's disease and Diminished quality of acetylcholine In conventional Medicine Perspective

Dementia
About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. Dementia is the loss of mental ability that is severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people. American typical diet contains high amount of saturated and trans fat, artificial ingredients with less fruits and vegetable which can lead to dementia and other kind of diseases.

Treatments
Depending to the causes of disease, most medication are to control the symptoms 
A. Alzheimer's disease and Diminished quality of acetylcholine
A.1. Treatments of mild and moderate Alzheimer's disease and Diminished quality of acetylcholine
1. Cholinesterase inhibitors 
a. Cholinesterase inhibitors are the primary treatment, including tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) for the cognitive symptoms of Alzheimer disease (AD). Dr. Trinh NH and the research team at the Massachusetts General Hospital, showed that for neuropsychiatric outcomes, 10 trials included the ADAS-noncog and 6 included the NPI. Compared with placebo, patients randomized to cholinesterase inhibitors improved 1.72 points on the NPI (95% confidence interval [CI], 0.87-2.57 points), and 0.03 points on the ADAS-noncog (95% CI, 0.00-0.05 points). For functional outcomes, 14 trials used ADL and 13 trials used IADL scales. Compared with placebo, patients randomized to cholinesterase inhibitors improved 0.1 SDs on ADL scales (95% CI, 0.00-0.19 SDs), and 0.09 SDs on IADL scales (95% CI, 0.01 to 0.17 SDs). There was no difference in efficacy among various cholinesterase inhibitors(1). Some researchers suggested that Persistent drug treatment had a positive impact on AD progression assessed by multiple cognitive, functional, and global outcome measures. The magnitude of the treatment effect was clinically significant. Positive treatment effects were even found in those with advanced disease(2). Some researchers suggested that if there is a decrease in the level of acetylcholine, a chemical messenger that assists memory, thought and judgment, then cholinesterase inhibitors may eventually lose their effect. In the article, Cholinesterase Inhibitors, posted in the Minister of health, the author(s) wrote that Cholinesterase inhibitors were developed to improve the effectiveness of acetylcholine either by increasing the levels in the brain or by strengthening the way nerve cells respond to it. Increased concentrations of acetylcholine in the brain lead to increase communication between nerve cells and may temporarily improve or stabilize the symptoms of Alzheimer's disease. These drugs appear to work best in the early and moderate stages of Alzheimer's Disease(3).

b. Side effects are not limit to
b.1. Nausea    
b.2. Diarrhea    
b.3. Vomiting    
b.4. Indigestion.     
b.5. Abdominal pain    
b.6. Loss of appetite
b.7. Fatigue
b.8. Weight loss
b.9. Etc.

A.2. Treatment of moderate and Severe Alzheimer's disease and Diminished quality of acetylcholine
a. Namenda® (memantine), an N-methyl D-aspartate (NMDA) antagonist are the most common medication used to moderate and Severe Alzheimer's disease.Scientists at the Brigham and Women's Hospital, Harvard Medical School, indicated that The key to memantine's therapeutic action lies in its uncompetitive binding to the NMDAR through which low affinity and rapid off-rate kinetics of memantine at the level of the NMDAR-channel preserves the physiological function of the receptor, underpinning memantine's tolerability and low adverse event profile. As the biochemical pathways evoked by NMDAR antagonism also play a role in PD and since no other drug is sufficiently effective to substitute for the first-line treatment of L-dopa despite its side effects, memantine may be useful in PD treatment with possibly fewer side effects(7). Others suggested that Moderate to severe AD. Two out of three six month studies show a small beneficial effect of memantine but not those in vascular dementia(8).

b. Side effects are not limit to
b.1. Confusion,
b.2. Dizziness
b.3. Drowsiness
b.4. Headache
b.5. Insomnia,
b.6. Agitation
b.7. Vomiting
b.8. Anxiety
b.9. Etc.
  
A.3. Other medication
3.1. Anticonvulsants
a. Anticonvulsants are a diverse group of pharmaceuticals used in the treatment of seizures, the clinical syndrome of Alzheimer's disease by suppressing the rapid and excessive firing of neurons that start a seizure. Some research suggested that Seizure pathophysiology may relate to increased amyloid beta-peptide production, structural alterations in neurones related to cytoskeletal dysfunction, cerebrovascular changes, neurotransmitter dysfunction or combinations thereof. Through modification of these pathophysiological pathways, there may be possible roles for anti-epileptic drugs such as sodium valproate and lacosamide in the treatment of Alzheimer's disease(4)

b. Side effects are not limit to
b.1. Dizziness
b.2. Drowsiness
b.3. Unsteadiness
b.4. Nausea
b.5. Vomiting
b.6. Skin rashes
b.7. Etc.

3.2. Sedatives
a. A sedative or tranquilizer is a drug that calms a patient, reducing irritability and excitement by by modulating signals within the central nervous system.The medication are highly addictive. Researchers at the Weill Cornell Medical College showed that antidepressant efficacy in BPSD other than depression (in particular, agitation, aggression and, occasionally, psychotic symptoms) do not influence prescription choices. Depressive symptoms may be taken more seriously in the absence of a previous history of depression, leading to increased antidepressant prescription rates in individuals presenting with depression for the first time(5).
 
b. Side effects are not limit to
b.1. Stomach upset
b.2. Blurred vision
b.3. Headache
b.4. Impaired coordination
b.5. Depression
b.6. Memory loss
b.7. Drowsiness
b.8. Etc.

3.3. Antidepressants
a. Antidepressant is a type of psychiatric medication used to treat depression, including mood disorder, dysthymia and anxiety disorders.In the study to assess the prevalence of antidepressant use in AD and to identify the clinical factors associated with antidepressant prescription, Dr. Arbus C, and the team at the Purpan-Casselardit Hospital, suggested that Antidepressant treatment was prescribed for 34.8% of patients. Clinically significant depressive symptoms (NPI >or= 4) were observed in 20.5% of the total population. Although depressed subjects were significantly more likely to be treated with antidepressants than non-depressed subjects (p<0.0001), only 60% of depressed subjects overall were prescribed an antidepressant. In multivariate analysis, clinically significant depressive symptoms were associated with antidepressant prescription although this result was only observed in subjects without a previous history of depression(6).

b. Side effects are not limit to
b.1. Dry mouth, 
b.2. Blurred vision
b.5. Drowsiness, 
b.4. Dizziness
b.5. Tremors
b.6. Sexual problems
b.7. Etc. 


Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/12517232
(2) http://www.ncbi.nlm.nih.gov/pubmed/19845950
(3) http://www.health.gov.bc.ca/pharmacare/adti/clinician/cholinesterase.html

(4) http://www.ncbi.nlm.nih.gov/pubmed/19557550
(5) http://www.ncbi.nlm.nih.gov/pubmed/20980585
(6) http://www.ncbi.nlm.nih.gov/pubmed/19735591
(7) http://www.ncbi.nlm.nih.gov/pubmed/21875407
(8) http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD003154.pub4/abstract;jsessionid=81B82BC5B10FAB9959A92CF39D439C21.d02t02

Dementia Preventions - Antioxidants Against Dementia

I. Dementia
About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. Dementia is the loss of mental ability that is severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people. American typical diet contains high amount of saturated and trans fat, artificial ingredients with less fruits and vegetable which can lead to dementia and other kind of diseases.

II. Antioxidants
Antioxidant is defined as a molecule inhibited the oxidation of other molecules by a chemical reaction that transfers electrons or hydrogen from a substance to an oxidizing agent in preventing the occurrence of oxidation. A free radical is any atom or molecule that has a single unpaired electron in an outer shell and highly reactive to react with other cell, which in turn, causes oxidative damage to the enzymes, other protein, unsaturated fatty acid, phospho-lipids, DNA and RNA, etc., leading to aging of the organisms, as a result of widespread damage due to set of a chain reaction auto-catalytically after attacking the lipid bilayers of the cell walls.

III. Antioxidants and Dementia
A. Antioxidant enzymes
Antioxidant enzymes are chemical substances found in plants that can protect the body from damage of free radicals by terminating the chain reactions by removing free radical intermediates and inhibiting other oxidation reactions.
1. Catalase
Catalase is an enzyme, found in most living organisms that are exposed to oxygen helped to converse hydrogen peroxide (free radicals) to water and oxygen as a rate of 40 million molecules of hydrogen peroxide to water and oxygen each second, using either an iron or manganese cofactor.

2. Glutathione peroxidase
The function of glutathione peroxidase is to protect the organism from oxidative damage by reducing lipid hydroperoxides, an oxidation of lipid cell membranes which can easily break and form free radicals of the form RO and converting free hydrogen peroxide to oxygen and water.

3. Glutathione reductase
Glutathione reductase, an enzyme reduces pair of sulfur atoms glutathione to the a organosulfur compound form of antioxidant (consisting of three amino acids joined by peptide bonds) which helps to prevent damage of important cellular components caused by free radicals and peroxides.

4. Super oxide dismutase (both Cu-Zn and Mn)
Super oxide dismutase is an important antioxidant defense in nearly all cells exposed to oxygen by converting superoxide into oxygen and hydrogen peroxide depending on the metal cofactor such as both Cu-Zn and Mn.

B. Metals binding proteins 
1. Ceruloplasmin
Ceruloplasmin, the major copper-carrying protein in the blood plays a role in iron metabolism. It prevents the oxidation that leads to the forming of oxidation from Fe2+ (ferrous iron) into Fe3+ (ferric iron) by exhibiting a copper-dependent oxidase activity, causing mutations in the ceruloplasmin gene cause of iron overload in the brain, liver, pancreas, and retina.

2. Ferritin
Ferritin, the protein produced by almost all living organisms, acts as a component to fight against iron deficiency and iron overload, keep in a soluble and non-toxic form and transport it to the body needs, including organs. It enhances the immune system in the presence of an infection or cancer and prevent the infectious agent attempts to bind iron to become free radicals by migrating from the plasma to within cells.

3. Lactoferrin
Lactoferrin, a multifunctional protein of the transferrin family, is one of the components of the immune system of the body by fighting against foreign invasion of bacteria and virus and lipid oxidation by inhibiting oxidation in a concentration-dependent manner even at concentrations beyond its capacity.

4. Metallotheinein
Metallotheinein, a family of cysteine-rich, low molecular weight proteins helps to bind both physiological heavy metals through the organosulfur compound of its cysteine residues. It also captures harmful superoxide and hydroxyl radicals by liberating the metal ions which were bound to cysteine.

5. Transferrin
Transferrin is a glycoprotein that binds iron very tightly but reversibly. It enhance the immune system in fighting against infection, inflammation by creating an environment low in free iron that impedes bacteria survival and cell oxidation.

6. Hemoglobin
Hemoglobin is the protein molecule in red blood cells that enhances the carrying of oxygen from the lungs to the body's tissues and return CO2 from the tissues to the lungs.
During oxidate stress, the cell membrane is protected by intraerythrocytic hemoglobin from the forming of free radical.

7. Myoglobin
Myoglobin is an iron- and oxygen-binding protein found in the muscle tissue of vertebrates. The binding of oxygen by myoglobin is unaffected by the oxidation or chain of oxidative reaction in the surrounding tissue, thus reducing the free radicals damage caused by oxidate stress.

8. Etc.


C. Common Free Radical Scavengers 
Bilirubin
Bilirubin is a prosthetic group which helps to break down molecules into smaller units in releasing energy, excreted in bile and urine. It is a cellular antioxidant, by reverting to biliverdin, a green tetrapyrrolic bile pigment, once again when oxidized that inhibits the effects of mutagens.

2. Carotenoids
Carotenoids are organic pigments, occurring in the chloroplasts and chromoplasts of plants and some other photosynthetic organisms like algae, some bacteria.
a. Beta-carotene
Beta-Carotene, an organic compound and classified as a terpenoid, a strongly-coloured red-orange pigment in plants and fruits.
a.1. It is not toxic and stored in liver for the production of vitamin A that inhibits cancer cell in experiment. Beta-carotene also neutralize singlet oxygen before giving rise of free radicals which can damage of DNA, leading to improper cell DNA replication, causing cancers.
a.2. Cell communication
Researcher found that beta-carotene enhances the communication between cell can reduce the risk of cancer by making cells division more reliable.
a.3. Immune system
Beta-carotene promotes the immune system in identifying the foreign invasion such as virus and bacteria by increasing the quality of MHC2 protein in maintaining optimal function of white cells.
a.4. Polyunsaturated fat
Researchers found that beta-carotene also inhibits the oxidation of polyunsaturated fat and lipoprotein in the blood that reduce the risk of plaques build up onto the arterial walls, causing heart diseases and stroke.
a.5. There are more benefits of beta-carotene.

3. Flavonoids
Flavonoids also known as Vitamin P and citrin are a yellow pigments having a structure similar to that of flavones occurred in varies plants. it has been in human history for over thousands of years and discovered by A. S. Szent-Gyorgi in 1930. As he used vitamin C and flavonoids to heal the breakage of capillaries, which caused swelling and obstruction of blood flow. Most plants have more than one group or type act as predominate.
Flavonoids process a property as antioxidants. it helps to neutralize many of reactive oxygen species (ROS), including singlet oxygen, hydroxyl and superoxide radicals.
Although nitric oxide is considered a free radical produced by immune system to destroy bacteria and cancerous cells, but when it is over produced, it causes the production peroxynitrite which may attack protein, lipid and DNA, Flavonoids inhibit NO production of peroxynitrite due to reduction of enzyme expression.

4. Vitamin A, C, E. D.
a. Vitamin A
Vitamin A occurs in the form retinol and is best known for its function in maintaining the health of cell membrane, hair, skin, bone, teeth and eyes. It also plays an important role as an antioxidant as it scavenges free radicals in the lining of the mouth and lungs; prevents its depletion in fighting the increased free radicals activity by radiation; boosts immune system in controlling of free radicals; prevents oxidation of LDL and enhances the productions of insulin pancreas.

b. Vitamin C
Vitamin C beside plays an important role in formation and maintenance of body tissues, it as an antioxidant and water soluble vitamin, vitamin C can be easily carry in blood, operate in much of the part of body. By restoring vitamin E, it helps to fight against forming of free radicals. By enhancing the immune system, it promotes against the microbial and viral and irregular cell growth causes of infection and inflammation.
Vitamin C also is a scavenger in inhibiting pollution cause of oxidation.

c. Vitamin E
Vitamin E is used to refer to a group of fat-soluble compounds that include both tocopherols and tocotrienols discovered by researchers Herbert Evans and Katherine Bishop. It beside is important in protecting muscle weakness, repair damage tissues, lower blood pressure and inducing blood clotting in healing wound, etc, it also is one of powerful antioxidant, by moving into the fatty medium to prevent lipid peroxidation, resulting in lessening the risk of chain reactions by curtailing them before they can starts.

5. Etc.

Alzheimer's Disease - My Story
This Is A Real Case Study, Written By An Alzheimer's Sufferer
Sharing His Hurts, Frustration And Desperation.


For the series of Alzheimer's disease, visit http://medicaladvisorjournals.blogspot.com/2012/01/alzheimers-disease.html

For Other Health articles visit http://medicaladvisorjournals.blogspot.com/
Sources

Delay Dementia - Do's and Do Not's List

I. Dementia
About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. Dementia is the loss of mental ability that is severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people. American typical diet contains high amount of saturated and trans fat, artificial ingredients with less fruits and vegetable which can lead to dementia and other kind of diseases.

II. Preventions
A. Do's and Do Not's list
 1. Mediterranean diet
If you are typical American dieter, you are at increased to develop dementia when you get older as the diet is classified as one of the most unhealthy diet in the existence, as the study of ,researchers wrote in an older population of Southern Italy with a typical Mediterranean diet, high monounsaturated fatty acids energy intake appeared to be associated with a high protection against cognitive decline. In addition, dietary fat and energy in older people seem to be risk factors, while fish consumption and cereals are found to reduce the prevalence of AD in the European and North American countries(1). Also recent research supports the hypothesis that calorie intake, among other non-genetic factors, can influence the risk of clinical dementia.(2).

2. Yoga 


Yoga is believed to have beneficial effects on cognition, attenuation of emotional intensity and stress reduction. In  the study to evaluate the effects of yoga on memory and psychophysiological parameters related to stress, comparing yoga practice and conventional physical exercises in healthy men (previously yoga-naïve). Memory tests, salivary cortisol levels and stress, anxiety, and depression inventories were assessed before and after 6months of practice. Yoga practitioners showed improvement of the memory performance, as well as improvements in psychophysiological parameters(3). Other researchers at the G.J. Patel Ayurved College, showed that Mind and body are inseparable entities and influences each other until death. Many factors such as stress, anxiety, depression, negative thoughts, unhealthy life style, unwholesome diet etc., disturb mental and physical wellbeing. Senile dementia is the mental deterioration, i.e, loss of intellectual ability associated with old age. It causes progressive deterioration of mental faculties, e.g., memory, intellect, attention, thinking, comprehension and personality, with preservation of normal level of consciousness.(4)




3. Aging of theory of mind
In the study to predict that educational level and cognitive processing are two factors influencing the pattern of the aging of ToM at Anhui Medical University, showed that  the younger group and the older group with equally high education outperformed the older group with less education in false-belief and faux-pas tasks. However, there was no significant difference between the two former groups. The three groups of participants performed equivalently in the eyes test as well as in control tasks (false-belief control question, faux-pas control question, faux-pas control story, and Eyes Test control task). The younger group outperformed the other two groups in the cognitive processing tasks(5)

3. Moderate alcohol drinking
Moderate alcohol drinking of less than 2 cups for men and 1 cups for women are said to offers possible health benefits(3), but Binge drinking in midlife is associated with an increased risk of dementia, according to the follow-up, 103 participants had developed dementia. Binge drinking (ie, alcohol exceeding the amount of 5 bottles of beer or a bottle of wine on 1 occasion at least monthly), as reported in 1975, was associated with a relative risk of 3.2 (95% confidence interval=1.2-8.6) for dementia. Passing out at least twice as a result of excessive alcohol use during the previous year, as reported in 1981, was associated with a relative risk of 10.5 (2.4-46) for dementia in drinkers.(6)

4.  Stop Smoking or never smoke before
Smoking is a risk factor for several life-threatening diseases, but its long-term association with dementia is controversial and somewhat understudied.In a studyof a total of 5367 people (25.4%) were diagnosed as having dementia (including 1136 cases of AD and 416 cases of VaD) during a mean follow-up period of 23 years. Results were adjusted for age, sex, education, race, marital status, hypertension, hyperlipidemia, body mass index, diabetes, heart disease, stroke, and alcohol use, Dr. Rusanen M, and the team at the University of Eastern Finland, said " heavy smoking in midlife was associated with a greater than 100% increase in risk of dementia, AD, and VaD more than 2 decades later. These results suggest that the brain is not immune to long-term consequences of heavy smoking"(6).

5. Drink you tea and coffee
Caffeine in tea and coffee may enhance cognitive function acutely. In Aging and Dementia (CAIDE) study, the findings of the previous studies are somewhat inconsistent, but most studies (3 out of 5) support coffee's favorable effects against cognitive decline, dementia or AD. In addition, two studies had combined coffee and tea drinking and indicated some positive effects on cognitive functioning. For tea drinking, protective effects against cognitive decline/dementia are still less evident. In the CAIDE study, coffee drinking of 3-5 cups per day at midlife was associated with a decreased risk of dementia/AD by about 65% at late-life. coffee(7).

6. Eat you fruits and veggies 
Fruits and veggies contains high amounts of antioxidant which enhance the immune system in fighting against forming of free radicals in which can cause damage to the brain cells of that lead to dementia. Researchers at The Johns Hopkins University indicated that use of vitamin E and vitamin C supplements in combination is associated with reduced prevalence and incidence of AD. Antioxidant supplements merit further study as agents for the primary prevention of AD(8).

7. Regular exercise and moderate exercise
 for elder
In the study to evaluate to the effects of regular exercise versus a single bout of exercise on cognition, anxiety, and mood were systematically examined in healthy, sedentary young adults who were genotyped to determine brain-derived neurotrophic factor (BDNF) allelic status, indicaed that altered activity-dependent release of BDNF in Met allele carriers may attenuate the cognitive benefits of exercise. Importantly, exercise-induced changes in cognition were not correlated with changes in mood/anxiety, suggesting that separate neural systems mediate these effects(9).

8.  Avoid nutritional deficiency with balance diet
a. Beyond our believe, in the study to highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease and a first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport.(10)
b. For more of the 8, please visit(11)

9. Avoid environment risk of dementia(12)
Certain environment toxins produced as a result of industrialization or naturally have been linked to cognitive degenerative diseases. Researchers at the University of British Columbia in the investugation of Novel environmental toxins: steryl glycosides as a potential etiological factor for age-related neurodegenerative diseases, showed that Mice fed washed cycad flour show signs that mimic ALS-PDC, which include progressive deficits in motor, cognitive, and olfactory functions associated with neuron loss in the spinal cord, nigrostriatal system, cortex, hippocampus, and olfactory bulb. Through a series of chemical extractions of washed cycad flour, we identified steryl glycoside molecules as bioactive molecules that are neurotoxic in culture and in mice. A detailed review of this class of molecule revealed that the molecules are abundant in the environment, particularly in plants and bacteria. Lipid analysis showed that some bacteria that are associated with some forms of neurodegenerative disorders have the capacity to synthesize steryl glycosides. Furthermore, certain steryl glycosides have been found to be a cell stress mediator and may have some immunomodulary effects. Others researchers showed that Parkinson disease (PD) and Alzheimer disease (AD), are of purely genetic origin in a minority of cases and appear in most instances to arise through interactions among genetic and environmental factors and early environmental origins of neurodegenerative disease in later life.

10. No illicit drug, please(13)
Illicit drug used may cause nervous system impairment as a result of direct and indirect effects on the integrity and function of nervous system tissue and, potentially, through immune effects. HIV-1 infection poses an additional risk of impairment, and this risk may be decreased as a result of antiretroviral drug treatment. Others researchers suggested that injection drug use represents the primary risk factor for up to 40% of patients with HIV infection.

11. Prevent prolonged period of using certain drug(14)
As aging, accumulation of toxins of certain medication used to treat certain diseases, such as antidepressants, sedatives, cardiovascular drugs and anti-anxiety medications may cause increased risk of cognitive dysfunction leading to produced dementia-like symptoms.

12. Etc.

Alzheimer's Disease - My Story
This Is A Real Case Study, Written By An Alzheimer's Sufferer
Sharing His Hurts, Frustration And Desperation.


For the series of Delay Dementia, visit http://healthyliving50over.blogspot.ca/p/delay-dementia.html

For Other Health articles visit http://medicaladvisorjournals.blogspot.com/

Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/12541015
(2) http://www.ncbi.nlm.nih.gov/pubmed/18466323
(3) http://www.ncbi.nlm.nih.gov/pubmed/22342535
(4) http://www.ncbi.nlm.nih.gov/pubmed/22408297
(5) http://www.ncbi.nlm.nih.gov/pubmed/22515730
(6) http://www.ncbi.nlm.nih.gov/pubmed/16222166
(7) http://www.ncbi.nlm.nih.gov/pubmed/20182054
(8) http://www.ncbi.nlm.nih.gov/pubmed/14732624
(9) http://www.ncbi.nlm.nih.gov/pubmed/22554780
(10) http://www.ncbi.nlm.nih.gov/pubmed/21402242
(11) http://healthyliving50over.blogspot.ca/2012/04/delay-dementia-causes-of-dementia.html
(12) http://healthyliving50over.blogspot.ca/2012/05/environment-toxin-causes-of-dementia.html
(13) http://healthyliving50over.blogspot.ca/2012/05/substance-abuse-causes-of-dementia.html
(14) http://healthyliving50over.blogspot.ca/2012/05/medication-causes-of-dementia.html

Friday, May 4, 2012

Delay Dementia - Symptoms and Complications of Dementia

I. Dementia
About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. Dementia is the loss of mental ability that is severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people. American typical diet contains high amount of saturated and trans fat, artificial ingredients with less fruits and vegetable which can lead to dementia and other kind of diseases

II. Symptoms and Complications of Dementia
Dementia is a neuropsychiatric disorder as a result of cognitive impairment and behavioral disturbances. The behavioral and psychological symptoms of dementia (BPSD) are common, contributing to caregiver burden and premature institutionalization. The true symptoms of dementia are a progressive loss of memory and other mental abilities of that can cause impairment of a person's ability to perform usual tasks in everyday life.
A. Symptoms
A.1. Symptoms of Alzheimer's disease 
Alzheimer's disease is a brain disorder named for German physician Alois Alzheimer. Alzheimer's destroys brain cells, causing problems with memory, thinking and behavior severe enough to affect language communication, memory, lifelong hobbies or social life. Alzheimer's gets worse over time, and it is fatal. Over 1 million people in US alone are currently afflicted by Alzheimer's disease because of degeneration of hippocampus and cerebral cortex of the brain where memory, language and cognition are located. With this mental disorder, brain cells gradually die and generate fewer and fewer chemical signals day by day resulting in diminished of functions. Overtime memory thinking as well as behavior deteriorates. Today, there is no know cure. 
In a study conducted by Hospital de Cruces, Plaza de Cruces s/n, Barakaldo of a total of 1014 patients (463 with higher and 551 with lower BPSD scores) were included (mean age 77 ± 7 years, 65% women). Almost all patients (90%) had BPSD at inclusion, 17% of which reported psychotic outbreaks. The most prevalent symptoms were lack of concentration (56%), tremors (56%), depression (44%), lack of cooperation (36%), and delusions (32%). Patients with higher BPSD scores showed a significantly higher prevalence of psychotic symptoms (delusions, hallucinations, and delirium) and tremors, while emotional symptoms (tearfulness and apathy) predominated in patients with lower BPSD scores. MMSE and ADAS-Noncog scores were negatively associated (p = 0.0284), suggesting a correlation between cognitive impairment and BPSD. Lack of concentration and appetite change significantly correlated with MMSE (p = 0.0472 and p = 0.0346, respectively). Rivastigmine and donepezil were the first choice therapies in mild to moderate dementia. ADAS-Noncog was generally considered better or similar to other scales (82%), and 68% of the investigators were willing to use it in the future.
Other symptoms include
1. Increasing forgetfulness
2. Communication difficulty
3. Depression
4. Anxiety
5. Mood and personal change
6. Difficulty making decision
7. Repeat question
8. Memory loss
9. Poor judgment
10. Etc.

A.2. Symptoms of Diminished quality of acetylcholine
If the nerves located in front of the brain perish, causing diminished quality of acetylcholine resulting in language difficulty, memory loss, concentration problem and reduced moblile skills because of lacking reaction in muscular activity and refection.
Symptoms of deficiency of acetylcholine include(2)
1. Difficulty remembering names and faces after meeting people
2. Difficulty remembering peoples birthdays and numbers
3. Difficulty remembering lists, directions or instructions
4. Forgetting common facts
5. Trouble understanding spoken or written language
6. Forget where I put things (e.g. keys)
7. Slowed and/or confused thinking
8. Difficulty finding the right words before speaking
9. Disorientation
10. Prefer to do things alone than in groups / social withdrawal
11. Rarely feel passionate
12. Feel despair and lack joy
13. Lost some of my creativity / lack imagination
14 Dry mouth
15. Etc.

A.3. Dementia due to long-term alcohol abuse
Dementia is common in patients with alcoholism. Although the symptoms of alcohol dementia are essentially the same as the symptoms present in other types of dementia, but there are few qualitative differences between alcohol dementia and other types of dementia. According to the article, "What's alcohol-related dementia?" The author(s) wrote" Alcohol dementia presents as a more global deterioration in intellectual function with memory not being specifically affected. Sufferers can present in their early thirties although the more common age for presentation is in the fifth, sixth and seventh decades. This condition is not, as suggested, a true dementia, in that recovery is possible. This seems to be more common in women and the recovery rates are better than for Korsakoff's Psychosis, provided correct support and alcohol abstinence is ensured. Most presentations are somewhere along the spectrum between Korsakoff's Psychosis and a global dementia. Others can present with damage to the frontal lobes to their brain which causes disinhibition, loss of planning, and executive functions and a blithe disregard for the consequences of their behaviour. Alcohol misuse can cause a general alcohol dementia that damages cells throughout the brain. Other types of alcohol-related dementia such as Korsakoff's Syndrome cause the destruction of certain areas of the brain, where changes in memory are the main symptom"(3)
Other symptoms include
1. Memory impairment
2. Language disturbance
3. Impaired ability to carry out motor activities despite intact motor function
d. Failure to recognize or identify objects despite intact sensory function
4.  Planning, organizing, sequencing, abstracting
5. Etc.

A.4. Multi-infarct dementia
Also known asvascular dementia , is the second most common form of dementia after Alzheimer's disease in older adults. It is caused by different mechanisms all resulting in vascular lesions in the brain. Major depression, depressed mood/anhedonia, and subjective and neurovegetative symptoms of depression that were unaccompanied by depressed mood/anhedonia in patients with clinically-diagnosed Alzheimer's disease (AD) and multi-infarct dementia (MID), as separate entities in AD and MID(4).
Symptoms include(5)
1. Confusion
2. Memory problems
3. Wandering Getting lost
4. Bladder incontinence
5. Bowel incontinence
6. Emotional problems
7. Laughing inappropriately
8. Crying inappropriately
9. Difficulty following instructions
10. Etc.

A.5. Dementia associated with Parkinson's disease
Parkinson disease (PD) is a disabling, progressive condition. It is a cognitive deficits due to the interruption of frontal-subcortical loops that facilitate cognition and that parallel the motor loop. Contrary to common perception, many Non-motor symptoms (NMS) of PD occur early in PD and some may even predate the diagnosis of PD that is based on motor signs. These include olfactory deficit, sleep problems such as rapid eye movement behaviour disorder, constipation and the more recently described male erectile dysfunction.(6). Other symptoms include(7)
1. Slow movement
2. Tremors
3. Rigidity
4. Poor balance
5. Constipation  
6. Difficulty swallowing  
7. Choking, coughing, or drooling  
8. Excessive salivation  
9. Excessive sweating  
10. Loss of bowel and/or bladder control
11. Etc.

A.6. Creutzfeldt-Jakob disease (CJD)
People who have eaten contaminated beef many years may be infected without even knowing it. Creutzfeldt-Jakob disease is a quickly progressing and fatal disease that consists of dementia, muscle twitching and spasm. CJD is characterized by rapidly progressive dementia. Initially, individuals experience problems with muscular coordination; personality changes, including impaired memory, judgment, and thinking; and impaired vision. People with the disease also may experience insomnia, depression, or unusual sensations.(8). Other symptoms include
1. Confusion
2. Depression
3. Lack of coordination
4. Strange physical sensations
5. Etc.

A.7. Subdural hematoma
It is the accumulation of blood beneath the outer covering of the brain that result from the rupture of blood vessel. Subdural hemorrhages may cause an increase in tracranial pressure, which can cause compression of and damage to delicate brain tissue. Acute subdural hematoma has a high mortality rate.
Other symptoms include(9)
1. A history of recent head injury
2. Loss of consciousness
3. Irritability
4. Seizures
5. Pain and Numbness
6. Headache
7. Dizziness
8. Disorientation
9. Weakness
10. Weakness or lethargy
11. Nausea or vomiting
12. Loss of appetite
13. Personality changes
14. Confused speech
15. Difficulty with balance or walking
16. Altered breathing patterns
17. Hearing loss or hearing ringing (tinnitus)
18. Blurred Vision
19. Deviated gaze, or abnormal movement of the eyes
20. Etc.

B. Complications
In the study conducted by Ichinomiya City Hospital, Ichinomiya, Japan, Dr. Ukai K,  and Mizuno Y. showed that Physical complications that occurred in our ward in the 12 months from April 2007 to March 2008 were recorded. Our ward has 50 beds and, over the 12 months, the average occupation rate was approximately 90%. We subdivided physical complications into two categories: (i) serious emergencies occurring in the ward with a possible high risk of mortality within a few days (e.g. pneumonia and upper airway obstruction); and (ii) life-threatening complications arising in the ward that required diagnosis and treatment by specialists from other medical departments (e.g. bone fracture and cancer)(10).
1. Pneumonia
In the study of Beth Israel Deaconess Medical Center, Boston, Massachusetts, Dr. Givens JL showed that Pneumonia is common among patients with advanced dementia, especially toward the end of life. Whether antimicrobial treatment improves survival or comfort is not well understood. The objective of this study was to examine the effect of antimicrobial treatment for suspected pneumonia on survival and comfort in patients with advanced dementia.(11)

2. Obstructive Sleep Apnea Syndrome (OSAS) 
The prevalence of OSAS increases with aging, occurring in up to 25% of older adults and up to 48% in patients with Alzheimer's disease. OSAS causes hypoxia, fragmented sleep, daytime sleepiness, cognitive dysfunction, functional decline, and brain damage resulting from reduced cerebral blood flow, ischemic brain lesions, microvascular reactivity, white matter lesions, and grey matter loss(12)

3. Bone fracture
In the study to investigate the relationship between bone mass and dementia in elderly hip fracture patients from areas with different aluminium concentrations in water supplies to determine  whether a high concentration of aluminium in the drinking water and the negative calcium balance of age-related osteoporosis together predispose to senile dementia.(13)

4. Urinary incontinence
Urinary incontinence may require insertion of a urinary catheter, which is known to increase the risk of UTIs. Urinary incontinence is a common problem in dementia. Almost invariably, the person with dementia will develop incontinence as the disease progresses. However, the primary reasons for incontinence are often not because of any significant pathology in the urinary system. Rather, it is due to factors outside the urinary system.(14)

5. Venous thromboembolism
In the study to assess  37988 patients of whom 1316 (3.5%) had dementia, Venous thromboembolism (VTE) patients with dementia had a high incidence of fatal pulmonary embolism (PE) and fatal bleeding. In those initially presenting with PE, the risk of dying of PE far outweighed that of fatal bleeding. In patients presenting with DVT alone, the risk of fatal PE was lower than that of fatal bleeding.(15)

6. Etc.

Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/18849899
(2) http://www.nutritional-healing.com.au/content/articles-content.php?heading=Acetylcholine%20deficiency
(3) http://neurology.health-cares.net/alcohol-related-dementia.php
(4) http://www.ncbi.nlm.nih.gov/pubmed/22164676
(5) http://www.rightdiagnosis.com/m/multi_infarct_dementia/symptoms.htm
(6) http://www.ncbi.nlm.nih.gov/pubmed/20642073
(7) http://www.helpguide.org/elder/parkinsons_disease.htm
(8) http://www.ninds.nih.gov/disorders/cjd/detail_cjd.htm#186463058
(9) http://www.nlm.nih.gov/medlineplus/ency/article/000713.htm
(10) http://www.ncbi.nlm.nih.gov/pubmed/20377817
(11) http://www.ncbi.nlm.nih.gov/pubmed/20625013
(12) http://www.ncbi.nlm.nih.gov/pubmed/20739254
(13) http://www.ncbi.nlm.nih.gov/pubmed/3239502
(14) http://www.ncbi.nlm.nih.gov/pubmed/16642241
(15) http://www.ncbi.nlm.nih.gov/pubmed/22374336

Nutritional Requirements for age of 50 and Over

 It has been recognized for some time that, for health and the normal functioning of the body, humans need to consume foods and drinks that are sources of energy (calories) and which together provide protein and contain a specific range of vitamins, minerals and trace elements. However, awareness is now growing of the provision by foods, especially plant foods, of a wide variety of substances that are yet to be recognized as nutrients as such, but which may confer health-promoting properties. These phytochemicals are represented in nature by various groups of structures that together include 3000-4000 individual compounds, and which possess a number of different properties(1).

Recommended daily intakes for micro nutrients as recommended by the Department of Health DRVs (Dietary Reference Values)(2)
A. Nutrient and                 Recommended daily intake for 50+ years 
1. Calcium (mg)                        700
2. Phosphorus (mg)                  550
3. Magnesium (mg)                   270
4. Sodium (mg)                       1600
5. Potassium (mg)                   3500
6. Chloride (mg)                     2500
7. Iron (mg)                               14.8
8. Zinc (mg)                                 9
9. Copper (mg)                            1.2
10. Selenium (μg)                      60
11. Iodine (μg)                         140
12. Vitamin A (μg)                   600
13. Thiamin (mg)                        0.8
14. Riboflavin (mg)                   1.1
15. Niacin (mg)                       12
16. Vitamin B6 (mg)                  1.2
17. Vitamin B12 (μg)                 1.5
18. Folate (μg)                      200
19. Vitamin C (mg)                 40
20. Vitamin D* (μg)                10

B. Estimated Average Requirements (EARs) for energy
Age (years), Estimated energy requirement for males (kcals per day), Estimated energy requirement for females (kcals per day)
51-59                      2550                                                                        1900
60-64                      2380                                                                        1900
65-74                      2330                                                                        1900
75+                        2100                                                                        1810

C. Proteins
Age (years)   Estimated protein requirement for males (kcals per day)   For females
51+                                            53.3                                                    46.5


Sources
(1) http://bmb.oxfordjournals.org/content/56/1/18.full.pdf
(2) http://www.milk.co.uk/page.aspx?intPageID=116





















Genetic Mutation causes of Dementia

I. Dementia
About 5-8% of all people over the age of 65 have some form of dementia, and this number doubles every five years above that age. Dementia is the loss of mental ability that is severe enough to interfere with people's every life and Alzheimer's disease is the most common type of dementia in aging people. American typical diet contains high amount of saturated and trans fat, artificial ingredients with less fruits and vegetable which can lead to dementia and other kind of diseases.

II. Causes of dementia
I. Genetic Mutation causes of dementia
Genetic mutation is defined as a condition of changes genetic structure and alteration in the inherited nucleic acid sequence of the genotype(1). there are always a concern of some dementia patient that the diseases may have been inherited and they will pass it on to their children.
1. linkage of Dementia with Lewy bodies (DLB) to 2q35-q26
In the study to investigate the second most frequent form of neurodegenerative dementia after Alzheimer's disease is dementia with Lewy bodies (DLB) and the relationship between DLB on chromosome 2q35-q36 in a multiplex,  Belgian family,researchers at the Department of Molecular Genetics, VIB, Antwerpen indicated that Possibly the disease mutation in this family acts through a more complex mechanism than generally envisaged for monogenic disorders. Nevertheless, identifying the first familial DLB gene is likely to contribute an entry point into the pathogenic cascades underlying DLB pathology.(2)

2. VCP R155H mutation
There are report from the researchers at the Ophthalmology and Genetics, University of Genova, that Italian family with multiple individuals diagnosed as having IBMPFD and carrying the recurrent R155H mutation. The implications for genetic counselling were also discussed, with regard to the procedures that may be offered to families suffering from a multisystem disorder with high risk of cognitive decline.


3. Genetic mutation and Alzheimer's disease
In the article of With Alzheimer's disease, 4 genes have been identified that affect its development. Three of these genes (the amyloid precursor protein (APP ) gene, presenillin gene (PSEN-1), and presenillin gene (PSEN-1)) affect younger people, while one other (apolipoprotein E (APOE )) affects older people.  It is important to note, however, that these genetic reasons for Alzheimer's disease are very rare and account for less than 1 in 1000 cases of the disease(4)

4. Chromosome 3 (FTD-3) caused by a truncating mutation in CHMP2B
Significantly decreased CBF was found in presymptomatic CHMP2B mutation carriers in occipital-and parietal lobes. Comparing SE with GRE, data indicate that FTD-3 vascular pathology might primarily affect brain capillaries(5).

5. Mutations in the NOTCH3
Mutations in the NOTCH3 gene are responsible for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), an adult onset hereditary angiopathy leading to ischemic stroke, vascular dementia and psychiatric disorders(6).

6. Etc.

Sources
(1) http://www.thefreedictionary.com/genetic+mutation
(2) http://www.ncbi.nlm.nih.gov/pubmed/20164589 
(3) http://www.ncbi.nlm.nih.gov/pubmed/18341608
(4) http://www.dementiaguide.com/aboutdementia/typesofdementia/geneticmutations/
(5) http://www.ncbi.nlm.nih.gov/pubmed/22422914
(6) http://www.ncbi.nlm.nih.gov/pubmed/22053260