Alzheimer Food List

Super Memory Formula

After the harsh reality that the doctor had to face his son ending his life, he suffered a major irreversible memory loss disease. This caused him to fall into depression and depend on the drugs from the pharma which was devasting for his mental and physical health and on so many other levels. After countless hours of research and experimentation, he realized that the root of all problems of memory loss was an enzyme that eats away the memory cells when the person gets older. This makes the person forget their loved ones, family and friends as if they have never met them. In some cases, they even forget about their past experiences, if they had children, how they came to the place they are in right now and who they are in the first place. This was exactly what the doctor had in his future if he did not make a decision. But he did and met with great people who helped him find the cure. This was a groundbreaking study that no one wanted to believe or endorse because it would go against the large pharma industry. However, the information is in there to protect yourself and your loved ones from such a devastating experience. You only need to follow the link and you will be guided to get the information downloaded to your device and follow the all-natural ways to get rid of memory loss. Read more here...

Super Memory Formula Summary


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Highly Recommended

This is one of the best books I have read on this field. The writing style was simple and engaging. Content included was worth reading spending my precious time.

Purchasing this book was one of the best decisions I have made, since it is worth every penny I invested on it. I highly recommend this to everyone out there.

Peroxisome Proliferatoractivated Receptor Ppary Agonists And Treatment Of Alzheimers Disease

Anti-inflammatory actions directed toward mitochondria. These agonists initiate a protective cascade that increases k(kappa)B expression and blocks NFK(kappa)B expression thereby reducing inflammatory gene expression and inflammatory responses. Therefore, PPAR-y is a novel therapeutic target for Alzheimer's disease that may reflect diverse affects, including improving energy metabolism, improving glucose uptake, and mounting an anti-inflammatory response. PPAR-y and the Treatment of Alzheimer's Disease To date, there have been two reported therapeutic trials of a PPAR-Y agonist to treat Alzheimer's disease. The first trial, conducted by our group, was a small pilot trial involving 30 persons with mild cognitive impairment or early Alzheimer's disease (98). The second was a much larger trial conducted in Europe with patients with Alzheimer's disease (99). Both trials showed therapeutic potential however, the trial by Risner et al. suggested that treatment effects are dependent on APOE...

Novel Treatment Strategies For Alzheimers Disease

In this final section, we will discuss three novel treatment strategies for Alzheimer's disease and for its prodromal stage, mild cognitive impairment (Table 1). The three strategies have a common thesis that improving insulin sensitivity will have a beneficial effect on patients with memory loss. Novel therapeutic strategies for Alzheimer's disease and mild cognitive Intranasal Insulin Administration and Treatment of Alzheimer's Disease We have previously reported that intravenous infusion of insulin facilitates memory and attention in patients with Alzheimer's disease and in healthy older adults (30). Therefore, this is a useful strategy to explore the effects of insulin on cognition, inflammatory responses, and A responses to increased plasma and brain insulin levels (43, 61, 80). There are, however, several practical issues that limit the usefulness of intravenous insulin infusion as a therapeutic strategy. One important limitation is that chronically raising plasma insulin levels...

Studies In Man Cognition And Dementia

Studies into the effects of diabetes on cognitive functioning in man can be broadly divided in two categories case-control studies, which are mostly cross-sectional, and population-based surveys, which are often longitudinal. The case-control studies usually involved selected populations of patients and matched nondiabetic controls, using performance on a battery of neuropsychological tests as an outcome measure. Population-based surveys mostly involved elderly subjects, and used either relatively crude cognitive screening tests or a clinical diagnosis of dementia as a primary outcome measure. Although, the risk of cognitive impairment in type 2 diabetes is well established, the underlying mechanisms remain largely unidentified. Type 2 diabetes typically develops in the context of a cluster of vascular and metabolic risk factors (including hypertension, dyslipidemia, and obesity), referred to as the metabolic syndrome. The metabolic syndrome itself, with or without hyperglycemia, is...

Mechanisms Linking Type Diabetes And Related Conditions To Mild Cognitive Impairment And Dementia

Detailed descriptions of the mechanisms linking T2D to cognitive impairment can be found in other chapters. This summary of mechanisms intends to put into perspective the epidemiologic evidence reviewed later in this chapter. We will classify the mechanisms linking adiposity, hyperinsuline-mia, and T2D to dementia as cerebrovascular and non-cerebrovascular. It seems fair to say that it is clearly established that adiposity, hyperinsuline-mia, and T2D are vascular risk factors, are accompanied by other vascular

Dementias Memory Loss

Memory loss is progressive with age but not due to aging. There are plenty of nonagenarians and centenarians with clear minds and good memories to prove that age is not the deciding factor in the dementias. Why do some people deteriorate much sooner Could you prevent personal deterioration of mental abilities You probably can. You will know it by noticing memory improvement. Telephone numbers that left you with no recall, unless you wrote them down, number by number, now form groups as you hear them, and you can jot them down the way you always did This is a good sign of memory improvement. Your writing can improve. The jagged, crooked, misaligned words can be smoothly written again You can remember things that happened earlier in the day and talk about it later, at mealtime. You can finish your thoughts in conversation.

Implications For The Prevention And Treatment Of Dementia

There is very strong evidence that adiposity, hyperinsulinemia, and T2D are related to cognitive impairment syndromes, whether AD, VD, or MCI, and whether the main mechanism is cerebrovascular disease or non-vascular mechanisms. However, more evidence is needed to establish causation. If the relation between these conditions and dementia were to be causal, the public health implications are enormous. As explained before, two-thirds of the adult population in the United States are overweight or obese, and the short-term trend is for this to worsen. These trends are also being observed worldwide. With increasing life expectancy we are likely to increasingly see the cognitive consequences of increased adiposity, hyperinsulinemia, and T2D in old age. We estimated that in New York City the presence of diabetes or hyperinsulinemia in elderly people could account for 39 of cases of AD (78). However, the other implication is that a large proportion of cases of AD could be preventable or...

Risk Factors For Dementia And Their Relation To Adiposity Hyperinsulinemia And Type Diabetes

Among environmental risk factors, diet (37), physical activity (32), and vascular risk factors (22) have attracted increasing interest. The evidence for various dietary factors is conflicting (37) and no solid conclusions can be drawn at this time. Higher caloric and fat intake may be related to a higher risk of dementia (38), and higher caloric and fat intake are related to increased adiposity (3, 4), hyperinsulinemia, and T2D. Several studies have found that increased physical activity is inversely related to dementia (39). High physical activity is typically accompanied by low adiposity (4), lower hyperinsulinemia, and lower T2D risk which may be the explanation for the beneficial effects. In terms of vascular risk factors, hypertension, dyslipidemia, diabetes, hyperinsulinemia, the metabolic syndrome, homocysteine, smoking, and heart disease are potential risk factors for Alzheimer's disease and vascular dementia (22). High adiposity, hyperinsulinemia, and diabetes are clearly...

Vitamin E and Alzheimers Disease

Research has shown that long-term use of anti-inflammatory medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) can lower the risk of Alzheimer's disease and help maintain cognitive function in patients with the disease. However, NSAIDs pose serious side effects and do not address the root of the problem. Hazardous free radicals, which go out of control when people fail to consume enough antioxidants, were implicated in the aging process back in 1954. Their role in damaging genes and cells is now generally accepted in medicine, and many Alzheimer's disease researchers believe that free radicals play a major role in the cognitive decline and behavioral changes characteristic of this disease. For example, amyloid beta protein, which strangles brain cells in Alzheimer's disease, releases large numbers of free radicals that injure brain cells, according to research by Ashley I. Bush, M.D., Ph.D., a neurology researcher at Harvard Medical School. In an experiment with brain...

Diet Exercise And Alzheimers Disease

We have reported that a 6-month lifestyle intervention resulted in physical and cognitive improvement in a sample of Japanese-Americans with impaired glucose tolerance (98). In brief, participants were randomized to receive either a low-fat diet paired with aerobic exercise (1 h three times per week active treatment group) or a typical American diet paired with stretching (control group). Relative to the control intervention, the active intervention reduced body mass index and increased the proportion of story information recalled after a delay. When we compared treatment-related changes in memory with treatment-related changes in glucose-stimulated plasma insulin levels (acquired at the end of a standard oral glucose tolerance test), improved story recall was associated with lower glucose-stimulated insulin levels, suggesting that memory improvement increased in conjunction with lower insulin levels (a marker of insulin effectiveness). Thus, diet and exercise can regulate both...

Diabetes And Dementia

Several well-designed epidemiological studies support the notion that T2DM likely increases the risk for dementia. Investigators in Honolulu Asia Aging Study reported that T2DM increased the incidence of Alzheimer's disease and vascular dementia among Japanese-Americans (20). Consistent with these findings, investigators for the Mayo and Rotterdam groups reported that the presence of T2DM increased the risk for Alzheimer's disease, independent of vascular dementia (21, 22) and Luchsinger et al. reported that hyperinsulinemia, a condition associated with early T2DM and impaired glucose tolerance, increased the risk for both memory impairment and Alzheimer's disease (15). Autopsy studies have not confirmed this relationship between Alzheimer's disease and T2DM (23). Therefore, diabetes may increase the risk for serious memory loss, presenting very much like Alzheimer's disease with a different pathophysi-ology than typical Alzheimer's disease. Convergent evidence supports the notion...

Epidemiologic Evidence Of The Relation Between Type Diabetes And Related Conditions To Mild Cognitive Impairment And

Few studies have explored the association between adiposity and AD, and several reveal conflicting findings. Elevated BMI in middle age may be associated with higher dementia risk (59, 60). A recent study showed that central adiposity in middle age was related to a higher risk of dementia in older age (61). Higher BMI at ages 70, 75, and 79 years may also predict higher dementia risk (62). However, there have been reports of no association at mid-life (63) and of lower BMI related to higher AD risk (64, 65) at older ages. There are several explanations for this apparent paradox. First, age of the adiposity measure in relation to clinical dementia onset varies across studies. Throughout life, there may exist critical periods in which risk or protective factors may have more or less impact. Second, several studies have reported weight loss preceding dementia onset (63, 66) that may precede diagnosis by decades (67). Understanding the reverse causality observed for adiposity parameters...

Diabetes Cognitive Impairment and Dementia

As with type 2 diabetes, the prevalence of cognitive impairment leading to dementia increases with advancing age (Park etal., 2003). Identification of any aetiological factors predisposing to cognitive decline is important in order to reduce the burden on patients, their carers and health and social services. Epidemiological evidence from both cross-sectional and longitudinal studies suggests that individuals with diabetes have a twofold increased risk of cognitive impairment and dementia compared with the general population (Areosa Sastre and Grimley Evans, 2003). This association between impaired cognition and diabetes appears to be strengthened by duration of the disease and the use of insulin therapy, likely reflecting illness severity in the case of type 2 diabetes. Longitudinal population-based studies confirm that diabetes is a risk factor for both vascular dementia and Alzheimer's disease (Peila etal., 2002 Areosa Sastre and Grimley Evans, 2003) Vascular dementia is a general...

Alzheimers Disease What Is Alzheimers Disease

Alzheimer's disease is the most common type of dementia. (The second most common form is caused by blood clots from ministrokes, a cardiovascular problem.) Alzheimer's is characterized by a serious impairment and worsening of memory, plus a decline in at least one other cognitive function, such as in perception or language skills. As Alzheimer's pro

Insulin And Dementia

Thus far, we have examined the relationship between insulin and normal memory, and now we turn to the relationship between insulin and dementia. As we have seen, diabetes increases the risk for both cognitive decline and dementia. It is important to keep in mind that T2DM represents both abnormal glycemic regulation and abnormal insulin activity. This section will examine the relationship between Alzheimer's disease, the most common form of dementia among older adults, and insulin abnormalities. First, we turn to a brief discussion on Alzheimer's disease. Then, we will turn to the discussion on insulin resistance and Alzheimer's disease. Alzheimer's Disease Dementia is a pathological condition characterized by deficits in memory, another area of cognitive functioning, and social or occupational functioning. The most common form of dementia among older adults is Alzheimer's disease. The most prominent symptom of Alzheimer's disease is a loss of declarative memory, which begins...


Other toxins are also present, such as aluminum, mercury, freon, thallium, cadmium. Aluminum buildup is seen in all Alzheimer's sufferers (100 ). This is undoubtedly part of the true cause. Did it come before or after the parasites Start a kidney cleanse (page 549) as soon as you can. Follow this with a liver cleanse (page 552). Clean up environment and diet. Your beloved family member or friend with Alzheimer's can regain her or his mental function to a considerable degree. Most important is stopping the mental deterioration before it is not reversible. Lisa Anne Reed, 60ish, was tentatively diagnosed with Alzheimer's 10 years ago. She needed complete care at present but was able to walk (could disappear quickly) and eat. She could occasionally say her name. Her brain had intestinal flukes and their eggs and Beth Hamm, 60ish, arrived led by her ever-vigilant, ever-caring husband. She was started by medical doctors on EDTA chelation to remove aluminum from her brain. My tests showed...

Determinants And Mechanisms

Genetic predisposition possibly plays a role in the association between type 2 diabetes, cognitive impairment, and dementia, but thus far only the role of the apolipoprotein (APOE) genotype and the Pro12Ala polymorphism of peroxisome proliferator-activated receptor-gamma (PPARG) genotype has been examined. The presence of the APOE s4 allele is a risk factor for the development of Alzheimer's disease (99). Patients with type 2 diabetes who carry the APOE s4 allele appeared to have a 2-fold increased risk of dementia compared to persons with either of these risk factors in isolation (100, 101). Data on the risk of cognitive impairment in non-demented persons are limited. Some studies reported an interaction with APOE where APOE s4 allele carriers who had diabetes had the highest risk of cognitive decline (14, 102, 103). Results of the Rancho Bernardo Study (32), Fig. 2. Relation between type 2 diabetes, related risk factors and cognitive decline. It shows a putative course of...

Psychiatric Comorbidity In Diabetes Mellitus Is There A Relationship With Cognitive Impairment

Other biomedical factors may also play a role, since it has been reported that depressive symptoms are related to white-matter abnormalities (35) and severity of diabetic complications (36). The association between white-matter abnormalities and depressive symptoms in older people has been labelled 'vascular depression' (37). Others refer to the co-occurrence of cognitive impairments, depressed mood, and vascular dysfunction as 'vascular dementia' (38) or 'pseudo dementia', i.e. geriatric depression with reversible cognitive deficits (37). The question of how psychological well-being is related to cognition or MRI abnormalities in type 1 diabetes has not been intensively examined yet. There are a few reports on a potential interrelationship between subclinical depressive symptoms, cognitive dysfunction, and MRI findings (10, 24). These studies failed to find a clear association between these variables in their participants.

Abduljalil Et Al. 2008 Eur J Pharmacol

Recommendations for the diagnosis and management of Alzheimer's disease and other disorders associated with dementia EFNS guideline. Eur J Neurol 2007 14 e1-e26. 106. Wessels AM, Scheltens P, Barkhof F, Heine RJ. Hyperglycaemia as a determinant of cognitive decline in patients with type 1 diabetes. Eur J Pharmacol 2008 585 88-96. 139. Areosa Sastre A, Grimley Evans J. Effect of the treatment of Type II diabetes mellitus on the development of cognitive impairment and dementia. The Cochrane Database of Systematic Reviews 2004 4.

Effect of Hypoglycaemia on Cerebral Blood Flow and Structure

Diagram Hypoglycaemia

Studies of the brains of people with diabetes using magnetic resonance imaging (MRI) demonstrated a high prevalence (69 in type 1 diabetes versus 12 in healthy non-diabetic subjects) of small periventricular high-intensity lesions known as 'leukoaraiosis' (Dejgaard et al., 1991). Leukoaraiosis is an age-related radiological finding that is also associated with hypertension, vascular disease, dementia and demyelination (Pantoni and Garcia, 1996). In a recent study using MRI, small subcortical white matter lesions were present in about a third of diabetic patients (Ferguson et al., 2003).

Assessment Of Cognitive Function

Corsi Block Weschler

One or more cognitive processes - or domains - exist. By establishing this pattern of cognitive deficits, we can subsequently relate this information to cerebral dysfunction in general or specific brain lesions. Although neuropsy-chological assessment in isolation can neither determine whether patients have organic lesions or not, nor accurately identify the side or site of the lesion, it provides information about cognitive function that can be interpreted in conjunction with other variables, such as neuroimaging findings or clinical history. For example, a person who performs poorly on a memory test does not necessarily have a memory disorder, since other non-cognitive factors may contribute to the task performance as well, such as motivation, or impairments in other cognitive domains, such as an attention deficit. However, if we know that this person is over 75 years, has had diabetes type 2 for over 15 years, shows a decline that has been progressive since approximately 2 years...

Riddle Mc Hart J. Hyperglycemia Recognised And Unrecognised As A Risk Factor For Stroke And Transient Ischemic Attacks.

Areosa Sastre A, Grimley Evans J (2003). Effect of the treatment of type II diabetes mellitus on the development of cognitive impairment and dementia (Cochrane Review). The Cochrane Library, Issue 4. Oxford Oxford Update Software. Barba R, Martinez-Espinosa S, Rodriguez-Garcia E, Podal M, Vivancos J, Del Ser T (2000). Poststroke dementia clinical features and risk factors. Stroke 31 1494-501. Haan MN, Mungas DM, Gonzalez HM, Ortiz TA, Acharya A, Jagust WJ (2003). Prevalence of dementia in older Latinos the influence of type 2 diabetes mellitus, stroke and genetic factors. Journal of the American Geriatrics Society 51 169-77. Honig LS, Tang M-X, Albert S etal. (2003). Stroke and the risk of Alzheimer disease. Archives of Neurology 60 1707-12. Munch G, Schinzel R, Loske C etal. (1998). Alzheimer's disease - synergistic effects of glucose deficits, oxidative stress and advanced glycosylation end products. Journal of Neural Transmission 105 439-61. Park HL, O'Connell JE, Thomson RG...

Insulin In The Periphery And The

Once in the brain, insulin regulates a variety of functions, including cognition. For example, our work has shown that an optimal insulin dose facilitates memory and attention in patients with Alzheimer's disease and in healthy older adults (30-34). In a typical experiment, we administered a fixed dose of insulin and a variable dose of dextrose, which allowed us to raise plasma insulin to postprandial levels and to maintain euglycemia. Under these conditions, patients and controls experienced an improvement in memory and selective attention. It may be argued that the infusion of dextrose actually accounted for cognitive facilitation however, results of two studies suggest that it is the insulin per se that is responsible for cognitive facilitation. In one study by Park and colleagues, insulin administered into the cerebral ventricles without glucose supplementation facilitated performance of a passive avoidance task (35). In a separate study, Craft and colleagues compared the...

Diagnosis And Ancillary Investigations

Diabetic Foot Drawing

A diagnosis of dementia is preferentially made in a multidisciplinary setting, based on clinical criteria (4, 5). These criteria include the presence of multiple cognitive deficits leading to a significant impairment in social and occupational functioning and a significant decline from a previous level of functioning. The clinical challenge is to define the aetiological diagnosis in an early phase, based on criteria such as those reviewed on the previous pages. This is crucial with regard to early initiation of therapy and optimal counselling of the patient and his family, especially when realizing that significant accumulation of neuropathology has taken place many years, even decades, before the first symptoms arise (42). When exploring cognitive complaints, a careful history is the basis for a good examination. A reliable informant is essential in this process, since the patient is often unaware of his own deficits. Important issues to assess in detail are premorbid functioning,...

Prediabetes And Cognition Prediabetic Stages

Global Atrophy The Brain

Are known to be associated with an increased risk of cognitive decline and dementia. In the next section the potential impact of these factors on cognition will be addressed. Population-based studies showed that persons with hyperinsulinemia, but no diabetes, have an increased risk for cognitive decrements compared to persons with normal blood insulin levels (40-43). The cognitive domains mostly affected were memory, attention, and mental flexibility. One study found evidence for greater cognitive decline over a 6-year period for persons with hyperinsulinemia compared to those without (43). The observed effects were at least partially independent of cardiovascular disease, hypertension, and other risk factors associated with the insulin resistance syndrome. Similar changes are observed in persons with poor glucoregulation. In the studies mentioned here, participants were classified as having impaired glucose tolerance according to the formal definition (36) or an abnormal glucose...

Relationship Between Depression And Cognitive Impairment

Similar to the relationship between diabetes and depression, dementia and depression have been closely linked and the directionality of this relationship remains uncertain (31, 73). Depression is highly prevalent among persons with dementia, and several studies have suggested that a history of depression may increase dementia risk. Volumetric changes of the hippocampus offer one possible explanation of recent findings that depression is a risk factor for dementia. Many patients with MDD report cognitive impairment, even in euthymic states. For example, when compared with controls, euthymic women with recurrent depression showed smaller bilateral hippocampal volumes and lower verbal memory scores, a neuropsychological measure of hippocampal function (74). Further, the severity of deficits correlates with total number of depressive episodes (75), and a smaller hippocampus, especially on the left, is predictive of incident dementia at 5-year follow-up in older depressed persons (76).

Measuring Cognition In Diabetes

The present chapter does not summarize the cognitive findings typical for diabetes type 1 and type 2. Nevertheless, we wish to address issues that need to be considered in order to design an optimal test battery for the assessment of diabetes-associated cognitive decline. Firstly, when patients with diabetes are compared with non-diabetic controls, effect sizes for the differences in performance between the groups are generally small (Chapters 10-12). This indicates that an optimal test battery should be very sensitive to be able to detect small changes in cognitive function and should not suffer from ceiling effects. Cognitive domains that are generally sensitive to brain dysfunction are speed of information processing and executive function, both requiring either fast or effortful processing. Furthermore, the impact of confounding factors should be kept to a minimum. In diabetes, potentially confounding factors are peripheral complications, such as neuropathy which may result in...

Laura A van de Pol Wiesje M van der Flier and Philip Scheltens

Introduction Types of Dementia Diagnosis and Ancillary It is estimated that within the next 50 years the number of patients with dementia in Europe will rise to over 16 million, due to increasing life expectancy in Western society. Besides the physical, social and psychological burden on carers of patients with dementia, the financial burden on society will grow exponentially too. Dementia is defined as an acquired impairment of cognitive function in at least two cognitive domains, including memory, which interferes with normal social or occupational performance. Dementia can be caused by various underlying diseases, the most common of which is Alzheimer's disease. The first part of this chapter will discuss the clinical signs and symptoms and neuropatho-logical findings of the most important types of dementia. An accurate diagnosis of a certain type of dementia is crucial for therapy and counselling of the patient and his family. Therefore, the second part of this chapter will review...

Therapies Targeted To Metabolic Pathways

Inos Ldiabetes

The tocopherols, especially the a-tocopherol isoform, have been promoted as effective antioxidant therapy for a number of neurological diseases, including Alzheimer's disease, epilepsy, cerebellar ataxia, and diabetic neuropathy. In studies of patients with diabetes vitamin E has been shown to decrease 8-isoprostane F2a (15), decrease low density lipoprotein-C oxidation at high doses (16), and increase skin blood flow and reduce free radicals in skin with topical application (17). Human studies of vitamin E using combined oral therapy with vitamin C, another well-established antioxidant have shown improved vascular function, but only in type 1 patients (18). Thus, vitamin E appears to exert antioxidant protective effects on neurons in diabetes although efficacy has not yet been demonstrated.

Medical Complications

During the first week after stroke onset, pressure sores are rare. They have been found in less than 1 of patients treated in a stroke unit (49), but in 27 of stroke patients in long-term units (61). Pressure sores can cause considerable pain and usually slow the patient's recovery. Immobilization is the most important cause. Previous stroke, previous trauma, and cognitive decline are also associated with an increased risk of pressure sores (61). Prevention relies on an early and accurate assessment of the risk to develop pressure sores. Prevention should include regular turning of the patient, relief of bony prominences, early mobilization, and adequate nutrition (62). The incidence of delirium after stroke has been reported between 13 and 48 . Delirium is more common after stroke than after myocardial ischemia, suggesting a causal relation between brain damage and the occurrence of delirium (72). Specific stroke types, such as large supratentorial infarcts, may be more likely to...

The Inflammation Syndrome Connection

The high-sugar and high-carbohydrate diets that lead to obesity raise glucose levels, and elevated glucose spontaneously generates large numbers of free radicals. These free radicals stimulate the inflammatory response, which can increase the risk of coronary artery disease, cancer, Alzheimer's, and many other diseases. In addition, abdominal fat cells secrete large quantities of pro-inflammatory interleukin-6 and C-reactive protein. In overweight and obese people both of these substances help maintain a state of chronic inflammation.

Studies In Man Therapies

Another interesting development, outside the field of diabetes, is the observation from a recent exploratory placebo-controlled trial in nondiabetic subjects with early AD that rosiglitazone, an insulin-sensitizing compound from the thiazolidinedione class, ameliorated cognitive decline (104). The effects of this compound on cognition were accompanied by an improvement of cerebrospinal fluid P-amyloid levels. Future studies should determine whether these compounds are superior than other classes of antihyperglycemic agents in preventing cognitive deterioration in patients with type 2 diabetes.

Counterregulatory Hormone Responses To Hypoglycemia In Older Adults

Matyka et al. (46), on the other hand, found differences in hypoglycemic symptom responses when comparing healthy older men, aged 60 to 70, with younger men, aged 22 to 26. During clamp studies, neuroendocrine responses for the two groups were similar. However, symptoms began earlier in the younger men and were more intense (46). Measures of psychomotor coordination deteriorated earlier in the older subjects and to a greater degree (46). The usual 10 to 20 mg dL plasma glucose difference between the subjective awareness of hypoglycemia and the onset of cognitive dysfunction was lost in the older men (46). This altered counterregulatory effect may contribute to the altered cognitive response to reductions in blood glucose. A lower glycemic threshold to hypoglycemia would be problematic in older persons. This would further limit the time available to self-treat and thereby increasing the risk of developing severe hypoglycemia (44,46). Additionally, in the older patient these...

Treatment Opportunities

Regarding the effects of improved glycemic control on cognition, it is difficult to disentangle the interplay between (1) patient factors, which demand a particular therapy, (2) potential direct effects of treatment on the brain, and (3) indirect effects of treatment on the brain, through modulation of glucose levels. This complex interplay, which prohibits inferences on causality, is clearly reflected in observations from the Rotterdam study, where patients receiving insulin treatment had the highest risk of developing dementia OR 4.3 (95 CI 1.7-10.5) , oral glucose-lowering medication was associated with an intermediate risk OR 2.4 (95 CI 1.4-4.1) and the lowest risk was found in patients who received no drug treatment OR 1.3 (95 CI 0.7-2.3) (152). It is yet uncertain whether reductions in the level of vascular risk factors will prevent cognitive decline in patients with type 2 diabetes. Studies in the general population thus far do not consistently demonstrate that modifications of...

Summary And Caveats Of The Evidence

The study of the association between adiposity and dementia is full of inconsistencies and caveats. The evidence could be summarized as showing that elevated adiposity in middle age is related to higher dementia risk, while the evidence for adiposity in older age is mixed. The epidemiologic evidence linking insulin resistance to dementia is limited by the small number of studies. Numerous studies have related T2D with a higher risk of dementia. The evidence is stronger for VD than for AD, which is expected given the status of T2D as a cerebrovascular risk factor. There are less studies relating T2D with MCI than there are relating T2D with dementia. They seem to indicate that type 2 diabetes is related both to amnestic MCI, thought to precede AD, and to non-amnestic MCI, thought to be more strongly related to cerebrovascular disease. Some studies show strong associations between T2D and AD despite taking vascular disease and stroke into account. However, the diagnosis of AD is usually...

Jos Alejandro Luchsinger

Conditions Risk Factors for Dementia and their Relation to Adiposity, Hyperinsulinemia, and Type 2 Diabetes Mechanisms Linking Type 2 Diabetes and Related Conditions to Mild Cognitive Impairment and Dementia Cerebrovascular Disease Non-Cerebrovascular Mechanisms Epidemiologic Evidence of the Relation Between Type 2 Diabetes and Related Conditions to Mild Cognitive Impairment and Dementia Summary and Caveats of the Evidence Implications for the Prevention and Treatment of Dementia Acknowledgments References hyperinsulinemia, with dementia. The mechanisms for these associations remain to be elucidated, but may include cerebrovascular and non-vascular mechanisms. Elevated adiposity in middle age is related to a higher risk of dementia. The evidence relating adiposity in old age to dementia is conflicting. Several studies have shown that hyperinsulinemia, a consequence of higher adiposity and insulin resistance is also related to a higher risk of dementia. Hyperinsulinemia is a risk...

Methodological Considerations

It is also critically important for researchers to be able to delineate, in a meaningful and reliable fashion, the neurocognitive characteristics of each child and any acute state - depression, anxiety, low blood glucose values -that might influence cognitive performance at the time of that assessment. Ordinarily, this is accomplished by administering a battery of psychome-trically sound neuropsychological tests, assessing mood state, and measuring blood glucose periodically during the assessment session. Unfortunately, there are no universally agreed upon standards for selecting such tests, particularly when assessing children (or adults ) with diabetes, despite pleas for the establishment of a core battery (5), as has happened in research with other neurocognitive disorders like dementia (6, 7). Lack of consistency in neuropsychological assessment across research groups challenges our ability to rationally aggregate results from many smaller cross-sectional studies.

Implications For Clinical Care

In the previous sections of this review we have summarized the results from studies on cognition and brain imaging in groups of patients with diabetes. How should these results be translated to the level of an individual patient who attends your clinic (Table 2) Obviously, not all patients with type 2 diabetes will experience changes in cognitive functioning and cognitive impairments in a patient with type 2 diabetes are not always due to diabetes. Moreover, while subtle cognitive decrements may be an early manifestation of dementia in the years to come, not all patients with cognitive impairments progress to frank dementia. deterioration, such as a neurologist or geriatrician to undergo more extensive physical and (neuro)psychological examination (Table 4). A neuropsycho-logical assessment can help to quantify the exact cognitive profile and severity of the problems. Diabetes is generally associated with relatively mild impairments, mainly in attention, memory, information-processing...

Conclusions And Directions For Further Research

The development of cognitive impairments in patients with type 2 diabetes appears to represent a continuum, with an onset in the pre-clinical stages of diabetes and a gradual progression thereafter. Although the data on cognitive decrements are difficult to translate to the individual patient, there is a substantial impact at the population level. Currently 6-8 of all cases of late-life dementia may be attributed to type 2 diabetes (68). Owing to the western lifestyle and aging of the population, the prevalence of type 2 diabetes is likely to increase and so is the incidence of cognitive decline and dementia attributable to type 2 diabetes.

Cognitive Functioning

Multiple diabetes-related comorbid conditions (i.e., hyperinsulinaemia, hypertension, hypercholesterolaemia) may individually and synergistically impact learning and memory skills see review by Ryan and Geckle (104) . For example, hyperinsulinaemia may independently affect the central nervous system. Insulin levels usually rise with age, and are strong predictors of cognitive impairment in adults without diabetes. Data from the Framingham study showed that both hypertension and diabetes independently affect cognition generally, and memory skills in particular. Given their high rates in type 2 diabetes, it is notable that hypertension and hypercholesterolaemia interacts with hyperinsulinemia to disrupt memory. Generally, there is evidence to support the view that verbal learning and memory skills are particularly vulnerable to disruption in type 2 diabetes compared with other cognitive skills as a result of diabetes and its comorbidities. Recent data has indicated a link between...

Fisoprostanes and overweight and obesity

Quantification of F2-IsoPs has been used to implicate a role for oxidative stress in the pathophysiology of a number of human conditions and diseases. Notably, F2-IsoP levels were shown to be increased in neurodegenerative conditions such as Alzheimer's disease, Huntington's disease, aging, certain types of cancers, and, of notable importance to consequences of overweight and obesity, atherosclerotic cardiovascular disease.1422-26

Dr Kunin and Susan Antioxidants for Health

One patient, Susan, had high blood pressure much of her adult life but opted not to treat it medically. By her late sixties she had undergone a triple coronary-artery bypass. She consulted Dr. Kunin after repeated attacks of angina (heart pain), arrhythmias after exercising, muscle aches, postoperative memory loss, bronchitis, and coughing. Memory loss is common after bypass surgery, and Susan had difficulty recalling her recent medical history.

Medications Monotherapy

Neurological manifestations include peripheral nervous system abnormalities of impotence, autonomic dysfunction, peripheral neuropathy, and postural hypotension central nervous system disturbances include behavioral changes, memory loss, hallucinations, nightmares, depressions, and insomnia.

What Else Might Help

Several other nutrients also might protect against cognitive decline and Alzheimer's disease. Acetyl-L-carnitine, 2 grams daily, has been found to improve attention spans, long-term memory, and verbal abilities in some Alzheimer's patients. Phosphatidyl serine, a phosphorus-containing fat, is essential for the health of cell membranes, particularly brain cells. Dosages of 300 mg daily have been found helpful in improving memory, but 100 mg also might work in mild cases of memory impairment.

Nutrients That Can Help

Animals, and people have found antioxidants to be of benefit. The most dramatic study, published in the New England Journal of Medicine, found that very high doses of vitamin E (2,000 IU daily) extended the ability of late-stage Alzheimer's patients to care for themselves. Researchers are currently investigating whether the same dosage of vitamin E can slow or reverse the early stages of Alzheimer's. However, if your mind is in good shape, 400 to 800 IU is probably sufficient for long-term prevention. A number of other antioxidant supplements might also be protective, including vitamin C, coenzyme Q10, and alpha-lipoic acid. Specific dosages are hard to determine because of the limited amount of research on these antioxidants and Alzheimer's disease. Extracts of the herb Ginkgo biloba also might be beneficial, though the research has been conflicting. Ginkgo serves as both an antioxidant and as a dilator of blood vessels in the brain, improving blood circulation to neurons. Some...

Psychological And Cognitive Function

Any level of psychological or cognitive deficit may lead to a poor or erratic diet affecting both nutritional state and glycaemic control. Memory lapses can result in missed meals and medication or an inadvertent repeated dose of some medications leading to, amongst other things, hypoglycaemia. Cognitive function is also impaired in people with diabetes due to increased incidence of cerebrovascular disease and depression (57,58). Psychological problems are both a predictor of mortality and of hospital admissions (59). Food intake can be markedly reduced in the presence of dementia. VOICES (Voluntary Organisations Involved in Caring in the Elderly Sector) produced a report in 1998 regarding the specific nutritional needs of elderly people with dementia (60).

Evaluating Intellectual Functioning

You need to evaluate the intellectual function of an elderly person with diabetes because managing the disease requires a fairly high level of mental functioning. The patient has to follow a diabetic diet, administer medications properly, and test the blood glucose. Studies have shown that elderly people with diabetes have a higher incidence of dementia (loss of mental functioning) and Alzheimer's disease than nondiabetics, making it much harder for them to perform these tasks.

Clinical Approach To Complaints Of Cognitive Dysfunction In Diabetic Patients

Assessment of the impact of changes in cognition on day-to-day functioning (for example problems with such activities as cooking, shopping, managing ones financial affairs, progressive dependence on spouse, social withdrawal, problems with self care, and medication use). Helpful screening lists have been developed to this end (105). Information on the presence of other diabetic complications and vascular risk factors, including blood pressure, is required. Prescription and nonprescription drugs, in particular analgesic, anticholinergic, antihypertensive, psychotropic, and sedative-hypnotic agents, should be reviewed carefully as potential causes of cognitive impairment. Alcohol use should be assessed. Laboratory tests can include a blood count, tests of liver, kidney and thyroid function, vitamin B12 levels, HbA1, and blood lipids. Brain imaging can be used to detect structural lesions (for example, infarction, neoplasm, sub-dural haematoma, and hydrocephalus), but can also contribute...

Noncerebrovascular Mechanisms

As described previously, one of the main consequences of adiposity is insulin resistance and hyperinsulinemia (2). The role of insulin in AD has attracted increasing attention (50) and is covered in more detail in Chapter 18. Insulin can cross the blood-brain barrier from the periphery to the central nervous system and compete with A for insulin-degrading enzyme (IDE) in the brain, including the hippocampus (51). Insulin is also produced in the brain and may alternatively have a beneficial effect on amyloid clearance (52). Peripheral hyperinsulinemia may inhibit brain insulin production which in turn results in impaired amyloid clearance and a higher risk of AD (52). Thus, it is possible that decreasing peripheral hyperinsu-linemia and increasing brain insulin levels have the same beneficial effect on AD. A study found that rosiglitazone, which decreases insulin resistance and decreases peripheral insulin levels, and is used in the treatment of T2D, may also be beneficial in...

Studies In Man Neuropathology And Brain Imaging

Up till two decades ago, studies on the structural basis of impaired cognition in man largely depended on neuropathology. Much has changed since the introduction of powerful neuroimaging techniques, such as computed tomography, and even more so Magnetic resonance imaging (MRI). Neuroimaging now plays a key role both in daily clinical practice and in cognition and dementia research. In patients suspected of dementia, MR in particular not only serves to exclude (rare) treatable causes of dementia, but increasingly adds to a more accurate diagnosis of dementia syndromes, also in the early stages (62). For research purposes structural and functional brain changes are evaluated More recent studies have assessed the relation between diabetes and the occurrence of neuropathological lesions that are common in AD, such as neurofibrillary tangles and amyloid plaques (68-70), but the results are inconclusive. Possibly, diabetes in interaction with the APOE e4 genotype leads to accelerated...

Mechanisms Contributing To Brain

Insulin Effects Insulin and Dementia Novel Treatment Strategies for Alzheimer's Disease Peroxisome Proliferator-Activated Receptor (Ppar-y) Agonists and Treatment of Alzheimer's Disease Diet, Exercise, and Alzheimer's Disease Summary References functioning. For example, diabetes increases the risk for memory loss, and treating diabetes can reverse memory loss. These studies have also identified a reciprocal relationship between insulin resistance and dementia, such that one condition increases the risk for the other. A substantial body of work has explored the role of insulin in regulating brain glucose metabolism, memory function, inflammatory responses, and amyloid concentrations. Knowledge of these relationships has suggested that increasing brain insulin activity may have a beneficial impact on memory and may serve as the basis for novel therapeutic strategies for Alzheimer's disease. Three such strategies include intranasal administration of insulin, drugs that improve insulin...

Interpretation Of Test Results

Both in clinical practice and in research settings, neuropsychological assessment typically has two aims the first is to contribute to the differential diagnosis of diseases or syndromes, the second is to provide information about cognitive strengths or weaknesses that can be used for decision-making with respect to treatment or care or educate the patient or his caregivers or significant others about neurocognitive changes that may be present. For making a reliable medical diagnosis, however, neuropsycholog-ical testing rarely contributes uniquely. While a low score on the MMSE is indicative for cognitive decline typically seen in Alzheimer dementia, a low performance may also be due to vascular cognitive impairments, Parkinson's disease, or even to problems in hearing. If cognitive tests or screening instruments are used for establishing medical diagnoses, information

Brain activity energy metabolism and neurotransmitter cycling

Epidemiological, cross-sectional and prospective associations between T2DM and moderate cognitive impairment of memory and executive functions have been discovered and were reviewed by Pasquier et al. (2006). Both vascular and non-vascular factors were found to be the reasons for dementia in diabetes (Stewart & Liolitsa 1999). Direct study using functional BOLD MRI of brain activation has shown that hypoglycaemia induced impairment of brain function is associated with task specific localised reduction in brain activation (Rosenthal et al. 2001). Higher increase of deoxygenation, depicted as higher BOLD signal in active brain areas, can help to overcome the energy shortage caused by hypoglycaemia (Rosenthal et al. 2001) or micovascular damage in type 1 diabetic patients (Wessels et al. 2006) with retinopathy. Certain overcompensation mechanisms can be observed in 31P and 1H MR spectroscopic observation of energy metabolism in type 1 diabetic patients, where, in contrast to healthy...

Diabetes And Neuropsychiatry Disorders

There is an emerging body of evidence that diabetes may accelerate age-related cognitive decline and leads to an almost twofold increase in the risk of both vascular and Alzheimer's dementia (21,22). An association with cognitive impairment has also been observed in pre-diabetic states of IFG (23), the metabolic syndrome (24) and insulin resistance (25). Diabetes may accelerate global cognitive decline, but psychomotor slowing has been reported as a characteristic finding in patients with diabetes (26). Although the increased prevalence of CVD may be a contributing factor, diabetes-associated dementia may occur independently of clinically significant micro or macrovascular disease (22,27). Proposed biological mechanisms for diabetes-associated central nervous system dysfunction include free radical-mediated oxidative stress, formation of advanced glycation end-products and alterations in neuronal insulin signaling pathways. In addition, a direct relationship between insulin metabolism...

Reactive Oxygen Species More for Tumor Cell Initiation Less for Metastasis Formation

ROS and RNS are closely linked to degenerative diseases such as Alzheimer's disease, Parkinson, neuronal death including ischemic and hemorrhagic stroke, acute and chronic degenerative cardiac myocyte death, diabetes mellitus type 2 and cancer. As a by-product of oxidative phosphorylation (mitochondrial respiration), a steady stream of reactive species emerges from our cellular energy plant, the mitochondria. ROS and RNS potentially cause damage to all cellular components. Structure alterations, biomolecule fragmentation, and oxidation of side chains are trade-offs of the cellular energy production. ROS and RNS production results in the activation of cyto-solic stress pathways, DNA damage, and the upregulation of JNK, p38, and p53. Incomplete scavenging of ROS and RNS, e.g. by the enzymes superoxide dismutase and catalase particularly, affects the release of mitochondria cytochrome c with subsequent activation of caspase 9 and 3 and ultimately induces the intrinsic death pathway.

School Performance

Performance on measures of verbal intelligence - particularly those that assess vocabulary knowledge and general information about the world - is frequently compromised in diabetic children (9, 14, 26, 40) and in adults (41) with a childhood onset of diabetes. The few studies that have followed subjects over time have noted that verbal IQ scores tend to decline as the duration of diabetes increases (13,15, 29). These effects appear to be more pronounced in boys and in those children with an earlier onset of diabetes. Whether this phenomenon is a marker of cognitive decline or whether it reflects a delay in cognitive development cannot yet be determined because sufficiently large numbers of diabetic and nondiabetic children have not been followed serially from childhood into early adulthood.


Food mold, particularly ergot, has the opposite effect of niacin. Brain blood vessels are made narrower, cutting down the oxygen supply. Ergot is a common contaminant of grains don't provide rye or pumpernickel breads or crackers. Don't provide wine or other alcoholic beverages they are too contaminated with ergot and aflatoxin. Narrowing the blood vessels in the brain can lead to stroke. If you notice Add vitamin C (1 8 tsp.) upon an attack of dementia coming, opening and wait 10 minutes try a niacin tablet (100 mg, not for it to act.

Scheltens Scale

Hummingbird Sign Mri

Atrophy in subjects with amnestic MCI is associated with a diagnosis of dementia at follow-up (48, 52). In the differential diagnosis between different types of dementia, the presence of hippocampal atrophy on neuroimaging is less useful, as hippocam-pal atrophy has been shown to be present in other types of dementia, such as FTLD, DLB and vascular dementia, as well (53-55). Frontal and temporal localized atrophy is suggestive of FTLD, although a normal MRI scan is not uncommon in this disorder (30). Semantic dementia is characterized by left-sided anterior, temporal lobe atrophy, and progressive non-fluent aphasia by left-sided perisylvian atrophy (30, 53). Some types of dementia show pathognomonic imaging features on MRI such as the characteristic marked hyperintensity of the caudate head and putamen that is seen in 70-80 of cases with sporadic CJD (56, 57) and the hyperintensity in the pulvinar in new variant CJD (57). PSP is associated with midbrain atrophy on midsagittal MRI,...

Borax Liquid Soap

Keep a dispenser by the kitchen sink, bathroom sink, and shower. It does not contain aluminum as regular detergents and soaps do, and which probably contribute to Alzheimer's disease. It does not contain PCBs as many commercial and health food varieties do. It does not contain cobalt (the blue or green granules) which causes heart disease and draws cancer parasites to the skin. Commercial detergents and non-soaps are simply not safe. Switch to homemade bar soap and borax for all your tasks Borax inhibits the bacterial enzyme urease and is therefore antibacterial. It may even clear your skin of blemishes and stop your scalp from itching.

Muscular Dystrophy

In muscular dystrophy the solvents, xylene and toluene are seen to accumulate in muscles. These also accumulate in brain and nervous tissue (See Alzheimer's page 269 and multiple sclerosis, page 204). Could it be that these solvents are actually present in the nerves of the muscles

Flukes and Solvents

The presence of xylene and toluene is associated in 100 of Alzheimer cases (over 10 cases) with the reproduction of intestinal fluke stages in the brain. There are many other flukes and many other diseases. Are there other fluke solvent disease trios Has fluke disease been going on for a long time or is it a recent phenomenon Certainly cancer is 100 years old, so is the use of propyl alcohol. Diabetes is quite old as an illness, too, and so is its associated solvent, wood alcohol. But HIV, AIDS and Alzheimer's are recent diseases. Should we conclude that benzene, xylene and toluene were used much less in the past


In DM1 patients treated with Exubera, the frequency of all hypoglycemic episodes was similar to those treated with SC regular insulin over 12 and 24 weeks of therapy (5.58 vs. 5.4 , respectively) (61,62). However, the rate of severe hypoglycemia defined as that requiring assistance by another, involving a neurological symptom (memory loss, confusion, irrational behavior, unusual difficulty walking, seizure, loss of consciousness) and associated with an SMBG 50 mg dL or in the absence of SMBG, that which was reversible with oral carbohydrate, SC glucagon or IV glucose was twice as frequent with insulin Exubera 6.5 vs. 3.3 RR 2.00 (CI 1.28 to 3.12) , compared with SC regular (87).


NF, consisting of heavy, medium, and light subunits, form the major structural lattice of axon. The function of the neurofilaments (NF) is not clear, but abnormal phosphorylation of these proteins is associated with neurodegenerative diseases such as amyotrophic lateral sclerosis, Parkinson disease, Alzheimer disease, and diabetes (58,59). In diabetes, stress-activated protein kinases are thought to be involved in their aberrant phosphorylation (60,61). Further, abnormal NF accumulation was found in the proximal axon segments of diabetic dorsal root ganglia sensory neurons in human (62), whereas loss of NF in distal nerve terminals of sensory neurons was observed in long-term diabetic rats (63). Impairment in the transport of NF proteins was suspected (64). However, it is not clear whether these changes are the cause or consequences of diabetic lesion.

Genetic risk

The population attributable risk (PAR) is important from a public health perspective but it does not tell us anything about individual risk. It describes the fraction of a disease that would be eliminated if the genetic risk factor was removed from the population. The population attributable fraction (PAF) is high in monogenic rare disorders like cystic fibrosis (around 50) but low for rare alleles in complex diseases. If the disease-associated allele is common, PAF increases. This is illustrated by the role of the Apo e4 allele in Alzheimer's disease and of the Pro12Ala polymorphism in the PPAR7 gene in type 2 diabetes. The PAF for Apo e4 in Alzheimer's disease is 20 because of the high frequency of the Apo e4 allele in the population (16 ). The PAF for the Pro12Ala polymorphism in the PPAR7 gene is even higher, 25 , as about 80 of the general population carries the risk allele Pro.

Lesson Sixteen

Development outdoors and in other animals. But if you become the total host so that various stages are developing in your organs, you have what I term fluke disease. I have found that cancer, HIV, diabetes, endometriosis, Hodgkin's disease, Alzheimer's disease, lupus, MS and universal allergy syndrome are examples of fluke disease.

Useful Resources

The Caroline Walker Trust distributes two guidelines relating to care of older people Eating Well for Older People and Eating Well for Older People with Dementia. Further information can be obtained from 22 Kindersley Way, Abbots Langley, Hertfordshire WD5 0DQ or

Wolfram Syndrome

Wolfram syndrome is the inherited association of childhood-onset diabetes mellitus and optic atrophy (38). As other complications were identified, the acronym DID-MOAD was coined (diabetes insipidus, diabetes mellitus optic atrophy, and deafness). This is a progressive, neurodegenerative disorder and many patients also develop urinary tract atony, ataxia, peripheral neuropathy, and psychiatric illness. We previously characterized the natural history of this condition in a UK nationwide series of 45 patients (39) (see Fig. 1). Diabetes mellitus presented at a median age of 6 yr, followed by optic atrophy at 11 yr. Optic atrophy is progressive, leading to vision of 6 60 or less in the better eye in a median of 8 yr (40). Cranial diabetes insipidus occurred in 33 patients (73 ), with sensorineural deafness (28, 62 ) in the second decade renal tract abnormalities (incontinence, neuropathic bladder 26, 58 ) presented in the third decade, followed by neurological complications (cerebellar...


In previous sections, we have discussed the relationship among insulin, insulin resistance, memory, and Alzheimer's disease. In this last section, we discussed three potential treatments for Alzheimer's disease based on our knowledge of the role of insulin in central nervous system functions intranasal insulin administration, PPARY agonists, and lifestyle modification (diet exercise). These three potential therapies have a common theme that improving insulin action should improve memory and may have an effect on neurobiological processes associated with age-related cognitive decline and Alzheimer's disease. Thus, these studies serve two important functions. First, they provide converging evidence that insulin resistance can be a pathogenic factor for memory loss and Alzheimer's disease and suggest several mechanisms to account for this relationship. Second, and perhaps most importantly, they use this knowledge to explore promising avenues for novel therapies for Alzheimer's disease.


In addition to changes in glucose metabolism, insulin also modulates levels of neurotransmitters, including acetylcholine, norepinephrine, and dopamine, which affect memory and attention. Acetylcholine is known to have profound effects on memory. For example, blocking acetylcholine receptors impairs memory (3). The observation that cholinergic neurotransmission is essential for memory forms the basis for the most commonly accepted treatments for Alzheimer's disease, namely cholinesterase inhibitors. At least one study has shown that low dose of insulin can ameliorate the amnestic effects of a cholinergic receptor antagonist (40). Insulin also modulates norepinephrine concentrations in rodent brains (41, 42). Collectively, these studies suggest that the insulin increases synaptic concentrations of norepinephrine by reducing reuptake by norepinephrine transporters. Recently, we reported that an intravenous infusion of a high physiologic dose of insulin yielded an increase in both...

Increase Oxygen

Brain problems include memory loss, communication deficit, dementia (calling things by inappropriate names and saying inappropriate things). The brain is simply not getting enough oxygen and food to work right. It is like having a pocket calculator with rundown batteries it will give you wrong answers (without telling you they are wrong). Not enough oxygen to the brain is the main cause of memory loss, inability to find the right words, getting words mixed up and not being able to speak in sentences. You can prove this by providing oxygen from a tank modern equipment is very easy to use and inexpensive. If your loved one responds well to a few hours of oxygen, you have proof of the problem.


With a parasite and pollution-free heart and a low-resistance, freely flowing kidney, some reserve strength will soon be built up. Weak spells are gone and forgotten. Your loved one is walking better, needing less sleep, and a golden age finally arrives. It is free of pain, free of medicine, free of shots and doctor visits, free of dementia, free of the dreadful weakness that demands so much help. They are free to enjoy family and friends again. Seeing themselves gain strength and be able to do more for themselves gives the elderly a sense of pride.

Mental effects

Cerebral atherosclerosis is more frequent in people with diabetes than in the general population. Patients may have one obvious stroke but multi-infarct dementia may be commoner than is generally recognized. Occasionally, prolonged, frequent hypogly-caemia can cause confusion or memory defects, or a state of paranoia which can be very hard to manage.

Glucose And Memory

The beneficial effects of glucose administration on memory have been well documented, as reviewed by Messier (4). Nearly three decades ago, Lapp demonstrated in teenagers that acute glucose administration could facilitate memory (5). Since then, researchers have shown in animals and humans that the beneficial effects of elevating plasma glucose levels on learning and memory are dependent on an optimal dose, the type of sugar, task demands, gender, age, cognitive status, and the relative timing of glucose administration and task (3, 4). These glucose effects are consistent with observations that the brain supply of glucose is derived from peripheral circulation and that glucose is the brain's principal energy substrate (6). Glucose-induced memory facilitation has been observed in both healthy older adult humans and persons with Alzheimer's disease (3, 7). For example, Craft et al. gave patients with Alzheimer's disease an oral glucose load of 75 g and showed improved memory for...

Neurological Changes

Elderly people may not have as many symptoms in response to hypoglycemia (tremor, sweating, fast heart rate, hunger), and so they may not recognize low glucose reactions as well as younger individuals do. This can cause a delay in treatment, and glucose levels can go dangerously low. If an elderly person is delirious because of an acute illness or is chronically confused because of dementia, his or her caregivers may have difficulty recognizing and treating low glucose reactions.

Subject Index

(ADAS-Cog), 449 Adiposity, 325 and AD, 331-332 and dementia, 328-329 elevation, 327 See also Alzheimer's disease (AD) Adrenocorticotrophic hormone (ACTH), 350 Adverse drug reactions (ADRs), 357 Age related cognitive decline and dementia role of insulin resistance, 434 brain insulin effects, 437-438 diabetes and dementia, 435-436 glucose and memory, 435 insulin and dementia, 438-439 in periphery and CNS, 436-437 Alloxan, usage, 390 Alzheimer's disease (AD), 105-107, 324 and adiposity, 331-332 diet and exercise, 449-451 and hyperinsulinemia, 332-333 and metabolic syndrome, 334-335 NINCDS-ADRDA criteria for 267-268 school performance, 254-256 See also Adults cognitive impairments, T1D Type 1 diabetes (T1D), in children and adolescents Cholecystokinin (CCK), 401 Cholinesterase inhibitors, in dementia treatment, 121, 438 See also Dementia Chronic hyperglycemia, in diabetic children and adolescents, 265-266 See also Type 1 diabetes (T1D), in children and adolescents Chronic inflammatory...

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