Memory, Sugar and Miasms
“Half of Americans said they were angrier than a year ago” according to one survey. We now have road rage, increased stabbings, one-punch brain injuries, revenge porn etc.; perhaps the world is getting angrier?
Other ills of modern society include an epidemic of obesity, type 2 diabetes, Alzheimer’s, etc.; is there a link, we might ask? One area of research is the effect of blood sugar levels on brain function – memory and cognition – and the search for a causative link to Alzheimer’s.
One such study, “Higher glucose levels associated with lower memory and reduced hippocampal microstructure”, published in the journal Neurology showed the ability to recall was weaker with increased levels of blood sugar, even though the blood sugar levels were within the “normal” range. The abstract explains the research:
Objectives: For this cross-sectional study, we aimed to elucidate whether higher glycosylated haemoglobin (HbA1c) and glucose levels exert a negative impact on memory performance and hippocampal volume and microstructure in a cohort of healthy, older, non-diabetic individuals without dementia.
Results: Lower HbA1c and glucose levels were significantly associated with better scores in delayed recall, learning ability, and memory consolidation…
Conclusions: Our results indicate that even in the absence of manifest type 2 diabetes mellitus or impaired glucose tolerance, chronically higher blood glucose levels exert a negative influence on cognition, possibly mediated by structural changes in learning-relevant brain areas. Therefore, strategies aimed at lowering glucose levels even in the normal range may beneficially influence cognition in the older population, a hypothesis to be examined in future interventional trials.1
There have been a number of research papers linking blood sugar levels with brain function, in fact, in 2005 the “disease” type 3 diabetes was introduced, none of which have been conclusive. Type 3 diabetes was posited as explaining Alzheimer’s. While there is a connection between blood sugar and problems of memory and cognitive function as in Alzheimer’s, there is not definite proof of causation. For example, a study published by the University of Pennsylvania in 2012 excluded people with a history of diabetes, indicating Alzheimer’s can develop without the presence of significant hyperglycaemia in the brain. This is in spite of the fact people with type 2 diabetes have an increased chance of developing Alzheimer’s, estimated to be between 50% and 65% higher.
Another recent paper shows that that reducing AGEs (Advanced Glycation End products) reduces the risk of Alzheimer’s and diabetes. The research from Mount Sinai Department of Geriatrics and Medicine’s press release reads as follows:
Advanced glycation endproducts, or AGEs, are compounds commonly found in the so-called “Western diet,” and previously have been linked to increased body weight, diabetes, and possibly Alzheimer’s disease. Now, researchers at the Icahn School of Medicine at Mount Sinai have shown that AGEs also cause brain changes similar to Alzheimer’s disease and pre-diabetes. AGEs, which naturally occur at low levels in the body, are found in high levels mostly in heat-processed animal food products, such as grilled or broiled meats; Mount Sinai researchers showed that consumption of such foods by mice raised the body’s level of AGEs, which, among other effects, suppressed levels of sirtuin, or SIRT1, a key “host defence” shown to protect against Alzheimer’s disease as well as metabolic syndrome, a pre-diabetic state.2
A fragmentary proving of Saccharum, the source of white sugar, did not elicit symptoms pertaining to memory or cognition, but symptoms of mood and temperament abounded:
Violent temper; irritable temper; quarrelsomeness,
Bilious sanguineous temperament,
Increased modesty of women,
Melancholic mood with the chilliness,
Low-spirited, hypochondriacal mood; peevishness,
Want of childish cheerfulness,
Indifference, as from homesickness,
Disinclination to talk; want of interest,
The substance showed a predominance of stomach symptoms in line with the sour, hot-headed symptoms of the mind:
Morbid hunger with the fever.
Nausea early in morning.
Vomiting of white, viscid, tough mucus.
Vomiting of blood; acid, making teeth dull; occasional, with the chill.
Stomach overloaded with sour mucus.
Digestion impaired; weak, with acidity.
Burning at pit of stomach.
Heat in stomach.
Coldness of stomach.
Pressure in stomach, morning, fasting.
Painful constriction of stomach.
Painful sensitiveness of pit of stomach.
So far nothing confirms Alzheimer’s or cognition problems result from sugar. Perhaps Alzheimer’s and diabetes are both due to another cause, like two branches on a tree. Type 1 diabetes, not fully understood, is due to the death of beta cells which produce insulin and Alzheimer’s is due to the death of brain cells, hence both have a common destructive tendency, a disposition, the fundamental cause of which Hahnemann called the syphilitic miasm.3
Type 2 diabetes throws up another complication. Patients with type 2 are prescribed the drug metformin (Glucophage) which blocks absorption of vitamin B12, a deficiency that causes memory loss and disorientation (as in diabetes). Furthermore, those prone to mature onset diabetes (type 2) are often over 60 and are likely to be deficient in B12 due to poor absorption of the vitamin resulting from a deficit of acid secretion in the stomach common in this age group.
With type 2 diabetes, either the body doesn’t produce insulin or the cells not respond to it, known as resistance. It may be due to “build up of amyloid.” Again the mechanism is not fully understood but initially, the body over produces insulin to get glucose into the cells, so that eventually sugar builds up in the blood leading to an increased breakdown of fats. In some case this may lead to metabolic syndrome: high blood pressure, excess fat around the waist and high blood glucose. Usually, the liver slows down the generation of glucose, but for some their livers continue to produce it; again, an over production. The italicised words indicate a golden thread of excess running through type 2 diabetes and its off-shoot, metabolic syndrome. For this disposition to excess, over production, Hahnemann posited a fundamental cause which he called the sycotic miasm.
The jury is still out on the role of blood sugar in memory health. It is evident other possible factors enter the equation: B12, diet, milk, heart disease, what one consumes their sugar with – coffee, breakfast cereals – the action of nitrates in food according to Dr de la Monte4, metformin etc., all of which illustrates medicine and science need to have a holistic approach to research and observation which includes acknowledging and incorporating as many connections as possible. When we consider the total phenomena, as Hahnemann would say, then we will understand disease in its entirety. Aside from the possible effects of excess sugar on the brain, there are grounds for considering it implicit in causing other harmful effects – on our mood.
1 Lucia Kerti, A. Veronica Witte, Angela Winkler, Ulrike Grittner, Dan Rujescu, Agnes Flöel, “Higher glucose levels associated with lower memory and reduced hippocampal microstructure”, http://dx.doi.org/10.1212/01.wnl.0000435561.00234.ee
2 Avoiding Harmful Byproducts of Heat-Processed Foods Protects Against Risk of Alzheimer’s Disease and Diabetes, http://www.mountsinai.org/about-us/newsroom/press-releases/avoiding-harmful-byproducts-of-heat-processed-foods-protects-against-risk-of-alzheimers-disease-and-diabetes
3 Because a disease might correspond to, for example, the syphilitic miasm, it doesn’t mean a homeopathic prescription will be a syphilitic remedy; the overall miasmatic state of the patient is what is prescribed on.
4 De la Monte, S. M., Neusner, A., Chu, J., & Lawton, M. (2009). Epidemiological Trends Strongly Suggest Exposures as Etiologic Agents in the Pathogenesis of Sporadic Alzheimer’s Disease, Diabetes Mellitus, and Non-Alcoholic Steatohepatitis. Journal of Alzheimer’s Disease : JAD, 17 (3), 519–529, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4551511/
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