This newsletter is the first of two parts which will be discussing some of the various natural treatments for Alzheimer’s disease (AD). AD is the most common form of dementia and is characterised by memory loss, difficulties with language, and motor and sensory functions. As the disease progresses changes in mood and behaviour increase. It is associated with an inability to carry out activities of daily life. The person affected is not usually aware of the memory loss. AD affects between 5 -10% of people over the age of 65 years; with the frequency rising with increasing age.
The clinical features of AD are believed to arise from cholinergic dysfunction (related to the parasympathetic part of the autonomic nervous system); by reduced activity of the enzyme choline acetyltransferase (which synthesise acetylcholine – involved in learning and short-term memory) and neuronal transfer of choline.
Most people agree that AD is associated with the death of neurons and that it is the loss of these neurons that results in the memory loss, social skills and poor cognitive behaviour seen in AD. The question is why does this occur and are we able to prevent this inevitable decline once the process of deterioration has been initiated?
There are various natural measures which have demonstrated some promising results (relating to improved mental function), in the early stages of AD.
Please note: In the advanced stages natural measures are of only limited benefit.
1) Diet: AD patients are more likely to have nutritional deficiencies. However it is still unclear whether these deficiencies are a secondary effect of the disease or due to poor eating behaviours. Either way a nutritional deficiency (as with most conditions) will compound and accelerate the deterioration. Dietary factors are clearly important with the prevention and treatment of AD. Diets rich in dietary antioxidants, fish (omega 3) and monounsaturated fatty acids (typically seen in the Mediterranean diet) appear to be associated with increased protection against cognitive decline. In contrast, to a diet high in saturated and trans fatty acids, cholesterol and low in dietary antioxidants may lead to an increase in serum and brain concentrations of aluminium (strong association with AD) and other transition metal ions, all of which are implicated in oxidative stress and may potentially lead to the neurological damage seen in AD. Poor quality diets may also increase the prevalence of AD by causing/increasing inflammation in the body, contributing to the neurological damage seen in AD.  
2) Nutritional Supplementation: The major fuel of the brain is glucose and a disruption in glucose utilisation is considered a significant factor in brain disease. The breakdown of glucose requires B group vitamins, zinc, magnesium and oxygen to ensure effective utilisation of the fuel. Many AD patients have shown to be deficient in these nutrients which may compound their problem, so it is no surprise since a deficiency in these nutrients in their own right can lead to dementia due to poor energy production. Poor energy production in neurons can be improved by ensuring an adequate supply of B group vitamins (particularly B1, B3, B6 and B12) as well as folate, zinc and magnesium. Other nutrients such as carnitine, lipoic acid and alpha keto glutarate have demonstrated an ability to improve mitochondrial energy production and therefore mental function.
Thiamine (vitamin B1) demonstrates some pharmacological effects on the brain. More specifically it “mimics” the important neurotransmitter involved in memory – acetylcholine. Thiamine has demonstrated an ability to mimic and increase the effects of acetylcholine in the brain. This effect explains the positive clinical results noted for thiamine (3 to 8 g/day) in improving mental function in AD (and age-related impaired mental function).  
Vitamin B12 is a key vitamin which has been linked to AD. A deficiency in vitamin B12 can result in impaired nerve function, causing numbness, paraesthesia, or a burning feeling in the feet, as well as impaired mental function, which in the elderly can mimic AD. Several studies have shown that the level of vitamin B12 declines with age and that vitamin B12 deficiency is found in 3% to 42% of persons aged 65 and older. Determination of vitamin B12 deficiency can be achieved by measuring the level in blood (serum cobalamin) or by the level of methylmalonic acid in the urine (for adenosylcobalamin). In addition, measuring the level of plasma homocysteine is emerging as a method of determining the status of vitamin B12 (and folate). There is a growing body of literature demonstrating a clear correlation between high levels of this marker and dementia and AD, (and cardiovascular disease). A study carried out at a Boston University, published in the New England Journal of Medicine concluded that high homocysteine levels (> 14 µmol/L) nearly doubled the risk of AD. In other studies, supplementation with vitamin B12 has shown tremendous benefit in reversing impaired mental function as a result of low levels of vitamin B12. It has been recently demonstrated that an oral daily dose as low as 50mcg can significantly increase serum vitamin B12 levels in vitamin B12 deficient elderly persons. Supplementation of B12 (or folic acid, or both) may result in complete reversal in some patients, but generally there is little improvement in patients who have had AD symptoms for more than 6 months, thus leading to the hypothesis that prolonged low levels of vitamin B12 may lead to an irreversible change that will not respond to supplementation. Methyl and adenosyl-cobalamin are forms of vitamin B12 that are active immediately on absorption and are therefore the preferred forms for supplementation.   
This is the end of part one of our Alzheimer’s disease newsletter. The second part will continue to look at more supplements which have demonstrated an ability to help in the treatment/prevention of (early) AD, such as zinc, phosphatidyl-choline/serine, L-acetylcarnitine, lithium orotate, antioxidants (e.g. lipoic acid, vitamin E, selenium and coenzyme), and omega 3 fatty acids, as well as socio-economic factors (which relate to the old saying – ‘bored brains shrink faster’).
Kingsway Compounding will be attending the Autism Exit Conference in Melbourne on this Monday (http://www.autismexit.org/events/conference-nov2011.php). We look forward to seeing you there if you are able to attend, it should be a great day.
I would also like to let you know of our trading hours over the Christmas holiday period for Kingsway Compounding. The compounding department will close from 1pm Thursday 22nd December 2011 and will re-open 9am Tuesday 3rd January 2012. We would appreciate it very much if everyone could place their orders early (at least 2 weeks before Christmas if possible) and at the latest by Friday 16th December 2011 to ensure all medications can be delivered before Christmas.
- Solfrizzi V, Panza F, Capurso A. The role of diet in cognitive decline. J Neural Tranm. 2003; 110: 95-110.
- Grant WB, Campbell A, Itzhaki RF, Savory J. The significance of environmental factors in the etiology of ‘alzheimer’s disease. J Alzeim Dis. 2002; 4: 179-189.
- Meador K, Loring D, Nichols M, et al. Preliminary findings of high-dose thiamine in dementia of Alzeimer’s type. J Geriatr Psychiatry Neurol. 1993; 6: 222-229.
- Benton D, Fordy J, Haller J. The impact of long-term vitamin supplementation on cognitive functioning. Psychopharmacol (Berl). 1995; 117: 298-305.
- Seshadri S, Beiser A, Selhub J, et al. Plasma homocysteine as a risk factor for dementia and Alzeimer’s disease. N Engl Med. 2002; 346: 476-483.
- Van Goor L, Woiski MD, Lagaay AM, et al. Review: cobalamin deficiency and mental impairment in elderly people. Age Aging. 1995; 24: 536-542.
- Nilsson K, Gustafson L, Faldt R, Gustafson L. Plasma homocysteine in relation to serum cobalamin and blood folate in a psychogeriatric population. Eur J Clin Invest. 1994; 24:600-606.