Why are all blood tests for vitamins meaningless?

Why blood tests for vitamins may not reflect the real picture

Blood is a transport, not a storage. Most vitamins circulate in the blood temporarily — their task is to deliver the substance from point A (for example, from the intestine or liver) to point B (to the cell, mitochondria, nucleus, etc.). It is not important how much vitamin is in the blood, but what happens to it next:

• Is it taken up by the cells?
• Is it converted into an active form?
• Does it work in metabolic pathways?

For example, vitamin B12 may be high in the blood, but the person experiences typical symptoms of its deficiency (fatigue, anemia, neurological disorders) because it does not enter the cells — due to a deficiency of the transporter or receptor dysfunction.

Impaired absorption in the gastrointestinal tract. If a person has:

• reduced stomach acidity (which hinders the release of vitamins from food),
• impaired function of the pancreas or gallbladder,
• problems with gut microflora or mucosa,

then vitamins, even when ingested through food or supplements, are not absorbed. In response, the body may even increase their release into the blood, but this does not mean that they work in the tissues.

This is especially characteristic of fat-soluble vitamins (A, D, E, K).

Impaired activation of vitamins. Many vitamins require enzymatic activation:

• Vitamin D needs to be activated first in the liver, then in the kidneys.
• B6 is activated with the help of magnesium.
• Folic acid (B9) must be converted into 5-MTHF (the active form).

If there is a failure at any stage of this pathway (for example, due to genetic mutations, as in MTHFR), then the vitamin will be in the blood but will not perform its function.

Cellular starvation despite sufficient blood levels. A classic example is insulin resistance: there is a lot of glucose in the blood, but the cell is "starving" because it cannot take it up. The same applies to vitamins. For example, in chronic inflammation, intoxications, or deficiency of carrier proteins, the cell may be unresponsive to the vitamin, despite its presence in the blood.

Alternative approaches:

• Assessment of clinical symptoms — the most reliable way.
• Functional tests — for example, homocysteine levels to assess the function of B12, B6, B9.
• Metabolite analysis — urinary organic acids, markers of mitochondrial activity.
• Accompanying tests — levels of carrier proteins, enzyme levels, levels of magnesium, zinc, and other cofactors.