Background – brain needs sugar
The brain is the major energy consumer in the human body (approx. 25% of the total energy consumption). This energy can easily be provided by the blood sugar (glucose). Just 150 years ago, sugar was a luxury good. Pure sugar meant reward and was used for special occasions in fine food. The supply of the body with glucose was ensured at that time by the nutrition from the simple and complex carbohydrates contained in numerous foods. From 1852 until today, however, the per capita consumption of refined sugar in Germany (as in all industrialised countries) has increased almost exponentially. This fact leads to a flooding of the body with sugars mainly in the form of fructose, glucose and sucrose.
Why does the brain need sugar?
Energy is required to maintain the structure and function of nerve cells. A mandatory fuel for the brain is the monosaccharide glucose, (simple sugar), also known as dextrose. Alternatively, the degradation products of fatty acids, the so-called ketone bodies (especially ß-hydroxybutyrate and acetoacetate) can be used by nerve cells as an energy supplier. Ketone bodies are formed, for example, in the starvation metabolism, during fasting or in the ketogenic diet. However, at least one third of the energy must be covered by glucose, which is about 40 g glucose per day. Both glucose or ketone bodies are converted within the cell into ATP (adenosine triphosphate), the energy carrier of all cells, and also provide substrates for cell construction.
Sugar overload – the Sweet Killer
Great, you might think: add as much sugar as possible and the brain (and all other cells) are full of energy!? Unfortunately, this is not true at all. The key point is the path that the glucose has to take to get from the blood and the extracellular space into the cell. The magic ingredient for this is the hormone insulin, which is produced by the pancreas and, as has been known for a few years, also to a lesser extent by the brain . Every cell has so-called insulin receptors that ensure that glucose is transported into the cell, but only as long as there is no insulin resistance.
Insulin resistance occurs when the sensitivity and response of the insulin receptors are disturbed and altered. Glucose can then no longer be adequately utilised, the blood sugar level rises and, above certain thresholds, the entire organism is immensely damaged. Insulin resistance leads to addictive behaviour (sugar addiction), fatigue syndrome, eating disorders, circulatory disorders and diabetes mellitus type 2.
What does insulin resistance mean for the brain?
The cells in the brain can also become insulin-resistant. However, the brain is the body’s largest energy consumer, so a lack of energy is catastrophic for all human cognitive and motor performance. Memory performance, cognitive abilities and concentration are particularly affected. Equally, the increased incidence of depression and dementia  is closely related to insulin resistance in the brain.
Insulin resistance is further increased by a lack of physical exercise. On the other hand, any kind of physical/muscular activity improves the sensitivity of the insulin receptors and facilitates the transport of glucose into the cell interior. Even serious cases of insulin resistance can be improved by sport and moderate exercise to a greater extent than by drug treatment .
But “grey is all theory…”. For those at risk of dementia, these facts provide some important recommendations:
- Eat a diet low in simple carbohydrates and sugar. A good method to achieve this is to follow the LOGI method (Low Glycemic Index). This form of nutrition does not exclude a piece of cake from time to time, but concentrates on low-carbohydrate vegetables and fruits, nuts, good meat (if desired, e.g. from cattle), lots of fish and good fats and oils (mono- and polyunsaturated fatty acids, medium-chain saturated fatty acids). But beware: Avoid dairy products! A similar concept is offered by the “Paleo (Stone Age) Nutrition”.
- In the kitchen and for sweetening, use sugars that have a less intensive effect on insulin levels: e.g. isomalutose, trehalose or selected sugar substitutes such as the sugar alcohol erythritol (see also further literature). Never use aspartame (trade name: NutraSweet®), which is suspected of causing neurological damage.
- Avoid industrially produced foods high in fructose, especially those made using the highly enriched corn starch syrup (HFCS/High-Fructose Corn Syrup).
- Supply the brain and the CNS with energy via D-galactose. About 6 – max. 12 g/day can easily be achieved as sweetness e.g. in espresso or tea.
- Use coconut oil in your diet. Coconut oil is excellent for frying and can be used as a substitute for butter or as a spread.
- Have your B-vitamin blood values measured and supplement if necessary. The more sugar (household sugar) you eat, the more vitamin B complex is needed to break it down. If there is a lack of usable B vitamins, the cell metabolism is literally “stuck” due to deficiency. The vitamins of the B group are all responsible in various ways for the release of energy and for certain brain and nerve functions. Vitamin B1 (thiamine), for example, is of central importance. A deficiency disturbs the entire carbohydrate metabolism and thus energy production. The first symptoms are increased irritability, fatigue and memory weakness. Vitamins B2, B3 and B5 are also necessary for energy conversion, while B6 (pyridoxine) is predominantly involved in brain function and B12 has essential protective functions for the nerve fibres in the brain and spinal cord.
- Gerozissis K. Brain insulin: regulation, mechanisms of action and functions. Cell Mol Neurobiol. 2003 Feb;23(1):1-25. doi: 10.1023/a:1022598900246. Erratum in: Cell Mol Neurobiol. 2003 Oct;23(4-5):873-4. Kyriaki Gerozissis [corrected to Gerozissis Kyriaki].
- Razay G, Vreugdenhil A, Wilcock G. The metabolic syndrome and Alzheimer disease. Arch Neurol. 2007 Jan;64(1):93-6.
- Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002 Feb 7;346(6):393-403.