Is consuming sugar a problem if you have Alzheimer’s? [ 02/02/11 ]
A diet high in carbohydrates with a high glycemic index* is thought by some experts to contribute to the risk for Alzheimer's disease. The arguments for this position include the following considerations:
- Most simply, a high sugar diet may increase the risk of obesity, and obesity is associated with harmful metabolic changes that increase the likelihood of Alzheimer's disease.
- High sugar intake can increase the risk for developing diabetes mellitus, a disease associated with increased risk for Alzheimer's disease.
- Even individuals without diabetes have been shown to develop altered sensitivity to insulin with high sugar intake, and one theory about Alzheimer's disease suggests that resistance to insulin's effects and lower levels of insulin-like growth factors in the brain may contribute to the development of this neurological condition.
Studies on animals have lent further support to the connection between sugar and Alzheimer's disease. Mice bred to be at high risk for brain changes resembling Alzheimer's disease showed memory impairment and higher levels of amyloid beta deposition in their brains when their water was sweetened with 10% sucrose. Evidence in human subjects suggests that a high sugar diet can interfere with cognition as well. Although the possible link between sugar and Alzheimer's disease might someday lead to development of a new treatment, it is already sensible for Alzheimer's disease patients (and truly for the rest of us as well) to monitor sugar intake and limit this to reasonable levels. Diets high in fiber, vegetables, nuts, and beans help regulate blood sugar and support health in a variety of ways. Further research will help to clarify the relationship between a diet high in carbohydrates that have a high glycemic index and Alzheimer's disease risk.
* High glycemic index means that the carbohydrates are broken down rapidly into glucose or blood sugar. They provide quick energy but contain few nutrients and little fiber, and in large amounts they may damage cells.
Is Singulair a safe drug to give someone who has dementia? [ 01/26/11 ]
Singulair is the brand name for montelukast, a leukotriene receptor antagonist used for maintenance treatment of asthma and for relief of seasonal allergy symptoms. By diminishing inflammation, montelukast helps asthma by reducing constriction of the airways. Its side effect profile includes a warning of increased risk for bleeding, and this might increase the risk for gastrointestinal bleeding that is rarely associated with cholinesterase inhibitors, which are used in the treatment of some dementias. Otherwise, montelukast's side effect profile and list of adverse reactions does not appear worrisome with respect to treating dementia patients.
My husband is in the middle stage of Alzheimer’s disease. His doctor has suggested adding lithium to his treatment plan, which currently includes Namenda and Aricept. Is lithium a new treatment for Alzheimer’s disease? [ 01/25/11 ]
Experiments reported in 2002 and 2003 showed that lithium inhibits an enzyme, glycogen synthase kinase. Researchers hypothesized that this action of lithium might reduce accumulation of beta amyloid and also block formation of neurofibrillary tangles by tau protein. Consistent with this hypothesis, experiments in cultured brain cells and in special transgenic mice have demonstrated that lithium reduces amyloid beta production in these experimental models of Alzheimer's Disease. Whether this property of lithium could translate into functional improvement in human victims of Alzheimer's Disease remains uncertain, but a 2007 transgenic mouse study (Caccamo et al. Am J Pathol 2007;170:1669-75) found lithium to reduce tau phosphorylation but not A beta or working memory deficits, and a single blind human study reported byHampel and colleagues in the Journal of Clinical Psychiatry (2009;70:922-31) found no treatment effect of lithium (at target blood levels from 0.5 - 0.8 meq/l during the 10 week trial) on global cognitive performance (measured by ADAS-Cog), depressive symptoms, GSK-3 activity, or CSF biomarker concentrations. At this time, lithium remains an agent of interesting possibilities but unproven human clinical benefit in the treatment of Alzheimer's disease.
Is losing the sense of smell a symptom of Alzheimer’s disease? If so, during which stage of the disease does this symptom occur? [ 01/21/11 ]
For several decades, researchers have recognized that impaired sense of smell is an early characteristic of Alzheimer's disease. The olfactory bulb and tract show degenerative changes early in the course of the illness, so investigators have developed "scratch and sniff" odor recognition tests in hopes of increasing early identification of Alzheimer's disease. These tests look for changes in the detection, identification, discrimination, and memory of odors. Since baseline olfactory measures are rarely available when such a test is administered to someone with a possible illness, it can be difficult to be sure that impaired ability to smell was not present all along. Furthermore, sometimes impaired sense of smell is the result of mechanical problems in the nasal cavity such as polyps or a deviated septum. The false positives (identification of people with impaired sense of smell but who do NOT have Alzheimer's disease) in smell tests have made this approach less popular than some more reliable diagnostic tests.
My mother was diagnosed with vascular dementia 4 years ago. Last September, she was moved from her older nursing home to a newer one that has a dedicated dementia unit, because the original home could not handle her anymore (she kept going outside and was disruptive with other patients). I have noticed a rapid decline since her move to this new nursing home, and I am wondering if this is just the progression of the disease or if the changes are related to her medications. I noticed changes immediately after she was prescribed Depakote, as she no longer made sense when she spoke. She is also on a very small dose of Seroquel. She has lost about 20 pounds in the past year, but she has been maintaining her current weight for about 4 or 5 months now. I would appreciate any information that you give me. [ 01/11/11 ]
The "non-cognitive behavioral symptoms" or NCBS of dementia often create more day to day difficulty than mere memory loss, as your mother's condition illustrates. She may need the attention of a skilled geriatric psychiatrist to sort out which of the many causes of disruptive behavior is most important in her particular case. Just as you point out, her disruptive behavior could reflect the progression of her dementia, the occurrence of a separate medical problem such as a stroke or a urinary tract infection, the development of a separate psychiatric problem such as depression (which is very common in this situation), the move to a new nursing home, the adverse effects of divalproex (Depakote) or quetiapine (Seroquel), or anxiety. With all of these choices, each of which would suggest a different course of action, some careful analysis must go into diagnosing your mother's condition. Her disease may make it impossible for her to rely on memory and new learning to improve her behavior, but a successful dementia unit often can apply behavioral methods to reduce disruptive behavior. If these fail, one or more of the available medications may be helpful. I hope this information will help you work with your mother's nursing home staff and a good consultant to improve her behavior and the quality of life for her and her caregivers.
I live in rural India, and my father was admitted to a hospital for an angioplasty. Subsequently, a blood clot developed, traveled to his brain and then dissolved. After that, he has exhibited classical signs of Alzheimer’s . After lunch, I give him .25 milligrams of alprazolam so that he can sleep, but this often does not help. After dinner, I give him .50 milligrams of the same medication, and this does seem to help him sleep through the night. He often has high levels of anxiety for approximately three hours before dinner and we don’t know how to manage it. The medicines prescribed to him by psychiatrists and neurologists increased his anxiety and prevented him from sleeping. He requires assistance in walking and changing. Should I increase his sedation? We tried giving him 1 milligram of lorazepam at night but it only disoriented him and kept him awake. [ 01/10/11 ]
I am sorry for your father's and your family's misfortune. His behavior may suggest Alzheimer's disease, but the occurrence of these symptoms after angioplasty and a clot to his brain suggests the possibility of vascular dementia as an alternative. Either way, the treatment of his anxiety appears to be the primary concern. Although I cannot give specific advice about the best medications for your father without knowing many more details of his health, I will suggest that you speak with his doctors to find a better approach than the use of alprazolam. This benzodiazepine sedative, like lorazepam, often reduces anxiety but at the same time interferes with aspects of mental functioning such as concentration and memory. Furthermore, a rebound anxiety may occur as one dose wears off and the next has not yet been given. Although behavioral approaches are considered the safest for addressing anxiety and agitation, many clinicians now also use antidepressants such as citalopram, antipsychotics such as quetiapine (though metabolic concerns may limit appropriateness of this choice), or anti-seizure medications to treat the symptoms you are describing.
My wife has been taking Namenda and galantamine for about 4 years. Is there any evidence that these medications are still working to slow the progression of her Alzheimer’s disease? [ 01/06/11 ]
Galantamine, the generic form of Razadyne, is a cholinesterase inhibiting medication approved by the FDA for treatment of mild to moderate symptoms of Alzheimer's disease (AD). Namenda, the brand name for memantine, works through a different mechanism that improves glutamate neurotransmission, and is also approved by the FDA for treatment of moderate to severe symptoms of AD. Studies have shown that these medications continue to benefit patients for at least up to 2 to 3 years. An encouraging study found benefits of combination therapy in AD patients followed for an average of 30 months, but we don't have enough information to prove that treatment for 4 years remains beneficial. Clinicians who continue these medications do so based on the absence of other helpful treatment approaches, the belief that such combination treatment is not harmful, and the possibility that continued treatment may help in various ways such as slowing cognitive deterioration, slowing loss of ability to perform activities of daily living, delaying the emergence of disruptive behaviors, and reducing caregiver burden. On the other hand, some patients and clinicians decide to discontinue treatment on the basis of unwanted side effects such as fatigue or dizziness, apparent lack of benefits, or cost considerations.
My doctor says that I have white flakes showing up in an MRI of my brain, but he did not explain further. What do the flakes mean? [ 01/06/11 ]
Your MRI may have shown 'flecks' of brighter areas on the MRI that reveal a condition called 'white matter disease.' There are many different causes of 'white matter disease,' and some are more serious than others. In older adults, disease of the small blood vessels can lead to characteristic 'white matter disease findings' on the MRI. When the small vessel disease is serious, it can be associated with cognitive changes, but the presence of mild white matter changes does not necessarily mean that severe cognitive impairment is present. Some causes of 'white matter disease' are treatable, so your doctor should discuss this finding with you further. Making the most likely diagnosis will require your doctor to consider your age and medical history as well as any current symptoms. He or she may also refer you to a neurologist for a more detailed further examination.