Alzheimer's and Parkinson's Diseases

Introduction

There are many conditions in Western industrialised societies today that were unheard of, or at least very rare, just a century ago. The same conditions are still unheard of in primitive peoples who do not have the 'benefits' of our knowledge. There is a very good reason for this: They eat what Nature intended; we don't. The diseases caused by our incorrect and unnatural diets are those featured on these pages.

Dietary causes

Alzheimer's:

Parkinson's:

Introduction

The declines in mental faculties as we get older, which are becoming increasingly common, are accepted as sad and heartrending, but 'normal': an inevitable consequence of old age. But this decline need never happen and should never happen. Senility and its associated conditions are yet more examples modern diseases which are very rare in primitive society and which are entirely preventable in ours.

Alzheimer's disease (senile dementia) and Parkinson's disease, which only really appeared in the last century, are the two most prevalent age-related degenerative brain disorders in Western societies. The degeneration of synapses and death of nerve cells are defining features of both. In Alzheimer's disease, neurons in the brain regions that control learning and memory functions are selectively vulnerable. In Parkinson's disease it is the dopamine-producing neurons in the brain regions that control body movements that selectively degenerate.

Studies of post-mortem brain tissue from Alzheimer's disease and Parkinson's disease patients have provided evidence that the conditions have similar causes to other diseases associated with the Metabolic Syndrome. Recent data suggest that both Alzheimer's disease and Parkinson's disease can manifest systemic alterations in energy metabolism (increased insulin resistance and deregulation of glucose metabolism, for example). Importantly, evidence is emerging that dietary manipulation can prevent these devastating brain disorders of ageing.

Alzheimer's disease

Alzheimer's disease makes up 55% of dementia cases in the UK, according to the Alzheimer's Society and over 800,000 people in the UK currently suffer the affliction. It is argued by some that the recent growth in numbers of people succumbing to Alzheimer's disease may be because it is a disease of the elderly and people are living longer. But that theory doesn't stand up to scrutiny as Alzheimer's disease is increasingly seen in younger people. Alzheimer's disease is also seen in people with other conditions known to be caused by an incorrect 'healthy' diet such as diabetes; and the number of people with Alzheimer's disease has more than doubled since 1980.

There is a disproportionate number of cases of deteriorations of memory, cognition, speech memory, working memory and visual-spatial skills among diabetics than non-diabetics; diabetics also have a two to three times increased risk of Alzheimer's disease compared to the general population.[1] [2] This may be down to the excessive levels of insulin, as Stolk and colleagues at Erasmus University Medical School, Rotterdam, The Netherlands, say that 'These findings are more compatible with a direct effect of insulin on the brain than with an effect through an increase in cardiovascular risk factors.' High-carbohydrate diets could lead to Alzheimer's disease through chronic over-exposure of cells to insulin signalling, which accelerates cellular damage in cerebral neurons,[3] and can cause insulin resistance.[4]

For nine years a research team followed 824 Catholic priests and nuns, 127 of whom had diabetes. [5] One hundred and fifty-one of them went on to develop Alzheimer's disease. Two thirds of those with Alzheimer's disease were diagnosed diabetics. Researcher Zoë Arvanitakis found that insulin in the blood stimulates a protein called 'tau' which tangles brain cells into Alzheimer knots. But the true causal factor is likely to be our 'healthy' diet as that is what stimulates the production of insulin and is also, of course, the cause of diabetes. Population studies tend to support this theory as they indicate that Alzheimer's disease is much more prevalent in diabetics across the world.

In a commentary in the medical journal, Lancet, Dr Mark Strachan reviewed research showing that, while normal levels of insulin have a significant effect on improving memory, high levels are associated with a significant decline in memory function. This suggests that the malfunction associated with insulin resistance leads to cognitive dysfunction because of insulin's inability to carry out its proper function.[6]

Alzheimer's disease could also be related to evolutionary factors. A gene, the apoE4 allele, for example, is nearly three times more frequent among Alzheimer's disease populations than the general population.[7] Table I shows the frequency of the apoE4 allele in various populations.[8] It illustrates that populations with a long history of agriculture have much lower frequencies of the apoE4 allele than are found in long-time, hunter-gatherer populations.

In consequence, populations with a long history of agriculture have more successfully weeded out the gene than northern Eurasian populations. This may be the reason why we are now succumbing to these diseases.

Low cholesterol and Alzheimer's disease

The low cholesterol we are all supposed to strive for is another likely cause of the increase on Alzheimer's disease. Work in the 1950s found that as we get older, the level of cholesterol in our brains declines.[9] Later studies suggested that this decline may be the cause of brain disorders such as Alzheimer's disease. In 1991, a paper discussing the relief of Alzheimer's Disease, asked that 'strategies for increasing the delivery of cholesterol to the brain should be identified' and recommended increasing fat intake.[10]

The Framingham Study added weight to this proposition when it examined the relationship between total cholesterol and cognitive performance.[11] Participants were 789 men and 1105 women who were free of dementia and stroke and who received biennial cholesterol checks over a 16- to 18-year surveillance period. Cognitive tests were administered four to six years after the surveillance period and consisted of measures of learning, memory, attention, concentration, abstract reasoning, concept formation, and organizational abilities. The researchers found a significant linear association between the level of blood cholesterol and measures of verbal fluency, attention, concentration, abstract reasoning, and a composite score measuring multiple cognitive domains. Participants with 'desirable' cholesterol levels of less than 5.2 mmol/L (200 mg/dL) performed significantly less well than participants with cholesterol levels higher than 6.25 mmol/L (240 mg/dL). Dr. Penelope K. Elias from Boston University said that 'It is not entirely surprising that lower cholesterol levels were associated with moderately lower levels of cognitive function, given [that] cholesterol is important in brain function.'

In view of this evidence, why on earth are the government so keen to get everyone on cholesterol-lowering drugs?

A third avenue also involves increasing fat intake. Two prospective studies reported that Alzheimer's disease is less prevalent among those who consume fatty fish; and other reports have linked low levels of omega-3 fatty acids in the blood with Alzheimer's disease. In an epidemiological study, Morris and colleagues in Chicago, Illinois, USA, reported that the number of cases of Alzheimer's disease was 60% lower in people who consumed fish once a week compared with those who rarely or never ate fish.[12] Although pathologists at the University of Washington, Seattle, and Vanderbilt University, Nashville, Tennessee, noted that analytical data implicated two omega-3 fatty acids, arachidonic acid (AA) and docosahexaenoic acid (DHA), as causal factors in the degeneration of brain cells.[13] Omega-3 fatty acids and fatty fish are recommended as part of a 'healthy' diet.

Starchy foods may be as much the cause of Alzheimer's disease as they are of diabetes. A report showed that a diet rich in saturated fats and low in carbohydrates can actually reduce levels of a brain protein, amyloid-beta, which is an indicator of Alzheimer's disease in mice with the mouse model of Alzheimer's disease.[14] The authors believe that insulin and a related hormone, insulin-related growth factor-1 (IGF-1), are the key players. They say 'Insulin is often considered a storage hormone, since it promotes deposition of fat but insulin may also work to encourage amyloid-beta production.'

This study runs counter to others which purported to show that high-fat diets had a negative effect on Alzheimer's disease. However, in an accompanying editorial, Dr Richard Feinman, editor of the journal, explains that 'Most studies of the deleterious effects of fat have been done in the presence of high carbohydrate.' In which case, and taking the vast amount of other evidence into consideration, isn't it conceivable that it is dietary carbs and not fats that are the causal factor?

Parkinson's disease

Parkinson's disease seems to have similar causes to Alzheimer's disease although it affects only about one-tenth as many people as does Alzheimer's disease. The symptoms of Parkinson's disease include muscle rigidity and tremor of the hands, which can become increasingly difficult to control as Parkinson's disease advances, particularly with the development of motor complications, such as end-of-dose wearing off and uncontrollable movement following long-term therapy.

There is much evidence that suggests a link between low levels of cholesterol and Parkinson's disease. The Rotterdam Study, involving 6,465 people aged over 55 examined over an average follow-up period of 9.4 years showed that this link was there.[15] Higher levels of total cholesterol in the blood were associated with a significantly decreased risk of Parkinson's disease. The highest risk was found with cholesterol levels below 6.1 mmol/L. Using that as a reference, they found that the risk dropped to 58% in the cholesterol range 6.1 and 6.8; it dropped to 46% between 6.8 and 7.4; and with a cholesterol level above 7.4 the risk was down to only 16%. Strangely, however, this link was only seen in women.

Treatment

The brain uses a disproportionately large amount of energy for its weight. It is usually thought that it needs to get this directly from glucose as it is unable to use fatty acids (breakdown products of fats) or amino acids (breakdown products of proteins). However, the principal sources of energy for brain are, in fact, acetic acid as well as ketones derived from dietary fats. Strictly chemically-speaking, neurons appear to source their energy not from glucose but from carboxylic acids, which are probably mostly derived from fatty acids, converted to ketones. Nevertheless, there appears to be an obligatory reliance on glucose to sustain normal function of brain as a whole, which may be because neurons cannot normally survive without the support of glial cells, which may only run on glucose.[16-17] Thus, the brain survives during periods of prolonged fasting by using energy derived ultimately from stored triglycerides (body fats), the glucose being derived from the glycerol the triglycerides are bound to.

During the 1990s, diet-induced high blood levels of ketones were found to be effective for treatment of several rare genetic disorders involving impaired use of glucose or its metabolic products by brain cells.[18] Other work also found that ketones protect neurons from a heroin analogue which induces Parkinson's disease, and a protein fragment which accumulates in the brain of Alzheimer's disease patients.[19] More than that, addition of ketones alone increased the number of surviving neurons which suggests that ketones may even act as growth factors for neurons.

We know that ketogenic diets are very effective treatments for many other chronic degenerative medical conditions. The evidence is that the Alzheimer's disease and Parkinson's disease may also be successfully treated and, more importantly, prevented with a low-carbohydrate, high-fat, ketogenic diet.

References

[1]. Leibson CL, et al. Risk of dementia among persons with diabetes mellitus: a population-based cohort study. Am J Epidemiol 1997; 145: 301-308.
[2]. Stolk RP, Breteler MM, Ott A, et al. Insulin and cognitive function in an elderly population. The Rotterdam Study. Diabetes Care 1997; 20, 792-795.
[3]. Henderson ST. High carbohydrate diets and Alzheimer's disease. Med Hyp 2004; 62: 689-700.
[4]. Rosedale R. Insulin and Its Metabolic Effects, Presented at Designs for Health Institute's BoulderFest, August 1999 Seminar http://www.mercola.com/2001/jul/14/insulin2.htm Accessed 8 December 2005.
[5]. Arvanitakis Z, Wilson RS, Bienias JL, et al. Diabetes mellitus and risk of Alzheimer disease and decline in cognitive function. Arch Neurol 2004; 61: 661-6.
[6]. Strachan, MWJ. Insulin and Cognitive Function. Lancet 2003; 362: 1253.
[7]. Bertram L, et al. The AlzGene Database. Alzheimer Research Forum. http://www.alzgene.org. Accessed 8 December 2005.
[8]. Lane RM, Farlow MR. Lipid homeostasis and apolipoprotein E in the development and progression of Alzheimer's disease. J Lipid Res. 2005; 46: 949-68.
[9]. Max Bürger. Altern und Krankheit als Problem der Biomorphose. 3rd Ed, Georg Thieme, Leipzig, 1957.
[10]. Corrigan FM, et al. Dietary supplementation with zinc sulphate, sodium selenite and fatty acids in early dementia of Alzheimer's Type II: Effects on lipids. J Nutr Med 1991; 2: 265-71.
[11]. Elias PK, et al. Serum Cholesterol and Cognitive Performance in the Framingham Heart Study. Psychosomatic Med 2005; 67:24-30.
[12]. Morris MC, et al. Consumption of fish and n-3 fatty acids and risk of incident Alzheimer disease. Arch Neurol 2003; 60: 940-946.
[13]. Montine TJ, Morrow JD. Fatty Acid Oxidation in the Pathogenesis of Alzheimer's Disease. Am J Pathol. 2005; 166: 1283-1289.
[14]. Van der Auwera I, et al. A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer's disease. Nutr Metab 2005; 2: 28.
[15]. de Lau LML, Koudstaal PJ, Hofman A, Breteler MMB. Serum Cholesterol Levels and the Risk of Parkinson's Disease. Am J Epidemiol 2006; 164: 998-1002
[16]. Ebert D, et al. Energy contribution of octanoate to intact rat brain metabolism measured by 13C nuclear magnetic resonance spectroscopy. J Neurosci 2003; 23: 5928-5935.
[17]. Takenaka T, et al. Fatty acids as an energy source for the operation of axoplasmic transport. Brain Res 2003; 972: 38-43.
[18]. VanItallie TB, Nufert TH. Ketones: metabolism's ugly duckling. Nutr Rev 2003; 61: 327-41.
[19]. Kashiwaya Y, et al. D-b-Hydroxybutyrate protects neurons in models of Alzheimers and Parkinsons disease. PNAS 2000: 97: 5440-4.