When a person begins to experience memory problems, it’s often carelessly said that they have developed Alzheimer’s disease. With current diagnostic criteria, about 70% of those affected are diagnosed with Alzheimer’s disease. The second most common type of dementia is vascular dementia. Below, I quote what is written about this disease on some websites.
Swedish Dementia Centre:
”Vascular dementia is sometimes called vascular dementia. Causes dementia by clots or hemorrhages restricting the oxygen supply to the brain. Even with vascular dementia, the damage can occur in different parts of the brain.”
1177 writes:
”Causes of reduced blood flow to the brain:
There can be several reasons for the blood flow to the brain to worsen. The blood vessels in the brain may have become narrow due to the deposition of fat, blood cells, and connective tissue on the inner vessel wall. Another reason for the brain getting too little oxygen is blood clots or hemorrhages in the brain, what is called a stroke.”
Hjärnfonden:
”Vascular dementia is caused by different parts of the brain not getting enough nutrients and oxygen.”
There can be several reasons for the blood flow to the brain to worsen. The blood vessels in the brain may have become calcified by the deposition of fat, blood cells, and connective tissue on the inner vessel wall over a long period.
The narrow vessels then prevent blood that carries oxygen from circulating sufficiently, and the lack of oxygen damages the brain’s nerve cells. Other reasons for the brain getting too little oxygen are blood clots or hemorrhages in the brain, i.e., a stroke. Untreated high blood pressure, smoking, diabetes, or heart disease can be causes of both stroke and worsening blood flow.”
National Guidelines from the Swedish National Board of Health and Welfare:
”Vascular dementia can debut suddenly and has a step-like progression caused by clots or hemorrhages in the brain, leading to oxygen deprivation and brain cell death.”
Comments on the explanations That vascular dementia is due to lack of oxygen seems to be agreed upon, but then it gets a bit vague:
- ”blood clots or hemorrhages…”,
- ”The blood vessels in the brain may have become narrow due to the deposition of fat, blood cells, and connective tissue on the inner vessel wall,” Where is the evidence for this claim?
- the brain not getting enough nutrients and oxygen. Nutrient supply can hardly be a problem since the nutrient molecules are much smaller than a red blood cell, which the latter, however, can get stuck in stiffened terminal arterioles.
- ”may have become calcified by the deposition of fat, blood cells, and connective tissue on the inner vessel wall,” Strange explanation that the vessel has become calcified by fat, blood cells, and connective tissue.
- ”Untreated high blood pressure, smoking, diabetes, or heart disease can be causes of both stroke and worsening blood flow.”
- ”caused by clots or hemorrhages” There it is, the same explanation as at the top.
Comments on the above
The explanations are too scattered, vague, and illogical to be accepted as acceptable explanations. To me, the explanations rather show that the cause of vascular dementia is not known. The only completely correct statement above is that ”the blood vessels may have become narrow” because that is precisely the cause of vascular dementia – blood vessels that become too ”narrow”. Let me explain how the blood vessels, or to be more precise, why the arteries have become narrow. Because it must be in the arteries where the blood is transported if the explanation for vascular dementia is oxygen deficiency.
It is the red blood cells that transport oxygen. Red blood cells have an outer dimension of 7-8µm. No problem for the red blood cells to pass through the arteries until they reach the very short thin terminal arterioles. These have an inner diameter of 2-10µm and form the outermost part of the arteries before they turn into capillaries. Now you surely understand what problems might occur in passing through a terminal arteriole that has lost its elasticity and resilience, because it must have these qualities to let red blood cells through in time with the heart’s pumping. When the heart’s pulse reaches a stiffened terminal arteriole of, let’s say, 2-5µm, it’s clear that it becomes difficult for a red blood cell of 7-8µm to pass through and enter the capillary. It and the following red blood cells might manage to get through, but there will be fewer red blood cells passing through the terminal arteriole per unit of time, and thus fewer red blood cells reach the capillary likewise per unit of time. This means that the amount of oxygen that can diffuse through the tissues (for that is how oxygen is delivered from the terminal arterioles to the individual cells) to individual cells decreases and in the end ceases entirely if the terminal arteriole has lost its elasticity and resilience.
Why can a terminal arteriole lose its elasticity and resilience?
All arteries, including arterioles, must have elasticity and resilience to be able to widen when the heart pumps the oxygenated blood and when the heartbeat is over, return to the initial state. The question then is how the elasticity and resilience in the arterial wall are maintained?
According to Furchgott, Ignarro, and Murad, who received the Nobel Prize in Physiology or Medicine in 1998, it is the endothelial cells, i.e., the inside of the vessels, that deliver nitric oxide NO to the smooth muscle layer (tunica media) located on the outside of the endothelial cells. Without NO, the tunica media stiffens, and then it depends on how much or little NO is delivered by the endothelial cells to the tunica media for how elastic or stiff the tunica media becomes. The nitric oxide comes from the oxygen in the air we breathe. But it is not the nitrogen in the inhaled air that is used for the production of nitric oxide. We exhale as much nitrogen as we inhale. Logically, the nitrogen comes from the food and drink we consume. Therefore, it is important that we eat things that contain a lot of nitrogen, for example, dark green and dark red above-ground vegetables.
The endothelial cells, which deliver NO to the tunica media, have a hairy exterior called the glycocalyx. Experimentally, it has been shown that the glycocalyx moves in time with the heart’s pumping, and this seems to be what signals the endothelial cells to transfer NO to the tunica media. Healthy glycocalyx (glycocalyx in homeostasis) is high and dense. Damaged glycocalyx (lost its homeostasis) is thus low and sparse.
To understand that it is better to have a high and dense glycocalyx than a low and sparse one, one can look at the wings of wind turbines. The longer the wings, the more power is generated by the rotation. It is the same with a high and dense versus low and sparse glycocalyx. There is more power from a high and dense glycocalyx to the signals that make the endothelial cells send NO to the tunica media.
Why can the high glycocalyx become low and sparse?
What can damage the glycocalyx? To understand this, one must first realize that the glycocalyx humans now have in their blood vessels is the result of hundreds of thousands of years or perhaps even millions of years during which the glycocalyx was exposed to food and drink that likely consisted of 1/3 each of the macronutrients fat, protein, and carbohydrates plus water and micronutrients in the form of vitamins and minerals from the fresh ingredients used during all those years. In this way, the glycocalyx achieved and maintained its balance (homeostasis) and if it had been disrupted by overindulgence or unbalanced eating during the day, the glycocalyx would recover during the at least half a day when people did not eat at that time but rested and slept.
We usually say that too much sugar is the cause
As much as we know, since we have moved away from the balanced diet (1/3 each of fat, protein, and carbohydrates) and let carbohydrates i.e., sugar, flour, and starch (which both turn into sugar on their way down to the small intestine) dominate both food and drink, metabolic diseases have skyrocketed. Whether it is the sugar or the pancreas’s increasing production of insulin with increased intake of sugar that damages the glycocalyx so that it loses its homeostasis and negative charge, we need not argue about. Together, they damage the glycocalyx.
My conclusion
Is that damaged glycocalyx leads to narrow terminal arterioles and reduced supply of red blood cells to the capillaries, which then cannot allow oxygen to diffuse to the memory center hippocampus in the brain’s command center to the extent that it should be able to do so that the cells can produce so much energy that the memory’s ”computers” can work with full power.
