It has been known for quite some time that a disturbance in blood glucose and insulin metabolism plays a central role not only in diabetes, but also in Alzheimer’s disease. When insulin, which is important for glucose utilization, can no longer work properly due to missing or damaged insulin receptors, the so-called insulin resistance occurs. This also applies to the brain, where it is called cerebral insulin resistance. If this occurs, our central nervous system may experience an energy deficiency despite high glucose levels in the blood. The resulting starvation state of the brain gradually leads to the cessation of its specific functions and the death of brain cells, which is particularly noticeable in the impairment of memory. Therefore, maintaining or restoring the energy metabolism of the brain is of crucial importance, especially at the beginning of Alzheimer’s disease.

And it is precisely at this point that the sister molecule of glucose could now come into play: galactose.

D-galactose, also known as mucilage sugar, is a simple sugar (monosaccharide) that is rarely found in food in its free form. As a rule, galactose is bound to other (sugar) molecules; for example, when bound to glucose (dextrose), forms the disaccharide lactose(milk sugar). As a component of lactose or of more complex oligosaccarides (sugar structures consisting of several simple sugars), D-galactose is predominantly found in milk and milk products from mammals. D-galactose is also present in plant foods such as legumes as a component of (mostly indigestible) oligosaccharides, although hydrolytic processes during soaking or cooking beans can result in the release of D-galactose in levels up to 180 mg/100 g dry weight in canned beans. Breast milk is considered unique in terms of its sugar content: it contains 55 – 70 g/l lactose and 5.0 – 8.0 g/l oligosaccharides. The latter are present in over 100 different forms, with D-galactose as the main component.

In the human organism, galactose occurs as a building block of oligo- and polysaccharides in various mucous membranes, from which the common name is derived. Bound to proteins and fats, galactose is an important building block of plasma membranes that protectively coat our cells. Galactose is particularly important for human development as a source of energy, but also as a structural element.

So how could an insulin disorder be circumvented by galactose?

One possible application of D-galactose could be in the treatment of cerebral insulin resistance, when cellular energy supply by glucose can no longer occur because of damage to the insulin receptor. The energy crisis in the brain could be avoided by ingesting D-galactose, since D-galactose can enter brain cells in an insulin-independent manner.

It has been successfully demonstrated in an animal model study: For this purpose, the animals were experimentally put into insulin resistance by chemically blocking the insulin receptors. The brains are then no longer sufficiently supplied with the essential energy substrate glucose. Neurodegenerative changes occur and the animals measurably lose their memory capacity.

Even more impressive was the fact that the addition of D-galactose to the drinking water not only remedied the cellular energy deficit, but also significantly improved the cognitive performance of the test animals. In contrast, comparison animals that drank pure water soon could not find their way to the food bowl. These effects were explained by the compensation of energy deficiency in the brain. In addition, D-galactose also stimulated the formation of a biomolecule called glucagon-like peptide 1 (GLP-1), which in turn increases cerebral insulin levels, but also has its own neuroprotective effects in the brain.

It now seems somewhat confusing that galactose is used in other experiments in healthy animals as a model substance for aging experiments. For this purpose, D-galactose is administered to the animals daily in high doses for several weeks parenterally, i.e., bypassing the gastrointestinal tract such as by infusion. This leads to neurodegeneration (simulating natural aging) and impaired neurogenesis in the hippocampus, which can thus be used as an experimental aging model.

So how can these contradictory results of galactose effects be explained?

  • D-galactose, at the dose used in aging studies, is more likely to impose an energy load in the long term in healthy animals and thus would have different effects than in pathological conditions such as Alzheimer’s disease, where energy deficiency exists.
  • Stimulation of GLP-1 secretion and associated neuroprotective effects occur after oral intake but are absent after parenteral D-galactose administration.
  • It cannot be excluded that galactose might have hormetic effects i.e., dose-dependent reversal effects in relation to (neurodegenerative) oxidative stress.

In addition to the extremely promising results in the Alzheimer’s animal model, there are now also numerous individual reports from patients on the positive effects of D-galactose. Werner Reutter, the head of the Alzheimer’s animal study, reported “initial attempts to offer D-galactose as a substitute to the starved brain cells of dementia patients. These proved promising in a number of patients. Orientation, memory and social communication improved significantly.”

Unfortunately, to date there is no clinical study that has scientifically investigated the therapeutic effect in AD patients of D-galactose and ruled out possible undesirable side effects. Neither the pharmaceutical industry nor health insurance companies seem to be interested in this. Why not? One can only make assumptions about this, perhaps because nothing can be earned with D-galactose, because it is not a drug, but “only” a sugar substitute. D-galactose is available without prescription and at low cost in pharmacies.

Werner Reutter’s recommendation:

With proven insulin resistance, one teaspoon of pure D-galactose in tea, water or coffee three times a day is sufficient. This dose should not be exceeded if possible. It is important to absorb galactose directly, and not to take the detour via pure lactose or milk (products). Lactose is first broken down into galactose and glucose in the small intestine. Galactose must be present in the blood at a higher concentration than is released by the digestion of foods containing lactose. Moreover, this digestive step is disturbed in about 10% of adult Central Europeans because they have lactose intolerance due to the lack of lactose-splitting enzyme.

The only contraindication is the presence of a congenital metabolic disorder of galactosemia, in which D-galactose cannot be metabolized and accumulates in the blood. However, this is already examined in infancy by the pediatrician (approx. 1 in 40,000 children). In case of positive findings, the administration of galactose is basically ruled out.

Conclusion:

A disturbance in blood glucose and insulin metabolism plays a central role not only in diabetes, but also in Alzheimer’s disease. This cerebral insulin resistance, which is also known as type 3 diabetes, leads to an energy crisis in the brain, which gradually results in the cessation of cognitive functions. D-galactose, the ‘sugar-sibling’ of glucose, is taken up by neurons in an insulin receptor-independent manner. Thus, it could be a nutritional way to normalize cognitive performance by balancing energy requirements under these deficiency conditions. This hypothesis has been successfully confirmed in animal models; unfortunately, a clinical study in demented patients does not exist to date. However, there are numerous promising patient experiences in which cognitive functions improved after energy-adapted D-galactose intake. Accordingly, D-galactose could be an effective and inexpensive means of regaining brain health in cases of cerebral insulin resistance.

References:

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