Do it twice a year! That's the bare minimum for your health! A blood count isn't enough! What tes...

The speaker argues that most people only look at total cell counts, but the real value lies in the indices. An elevated MCV signals insufficient DNA synthesis from lack of B vitamins, while a low MCV points to iron or molybdenum shortage. The white blood cell differential acts as a quick decision tool for infectious illness: a lymphocyte rise means the body is fighting a virus—antibiotics are useless, so the patient should rest, take vitamins, and eat chicken soup. A neutrophil (granulocyte) spike with red, pus-covered throat is likely streptococcal angina and may need antibiotics if natural methods fail. Eosinophil elevation should trigger a search for parasites or allergies, possibly with a naturopath or an open-minded physician, or even by the patient themselves if they are self-diagnosing. This transforms a rudimentary test into a practical self-care guide.

The speaker stresses that relying on fasting glucose alone is a major failing of routine care. By the time fasting glucose rises, beta-cell dysfunction is far advanced. Instead, he advocates checking glucose and insulin one hour after eating. A typical scenario: glucose within normal range, insulin well above the upper limit → insulin resistance. He also introduces the next diagnostic layer: the autoimmune panel (anti-GAD, anti-IA-2, anti-ZnT8) reveals that many older patients diagnosed with type 2 diabetes actually have slowly progressing type 1, which requires a different treatment approach. This dual message—test postprandially and don’t stop at glucose alone—aims to help people catch dysfunction years earlier and avoid misdiagnosis.

The speaker flips the conventional focus: instead of measuring the active hormone, he stresses the prohormone 25-OH-D3 because the 1α-hydroxylase enzyme, once believed to reside mainly in liver and kidneys, is now known to be widely distributed—in brain, pancreas, endothelium, endocrine glands, gonads, breast tissue, and kidneys. This means each tissue can locally convert the prohormone to its active form to meet its own needs. If 25-OH-D3 is low, those tissues are starved of substrate, even if circulating active vitamin D remains adequate. He adds that sick individuals often maintain normal 1,25-dihydroxy D as a compensatory mechanism, so that test can give false reassurance.

The speaker devotes considerable time to the issue of manipulated reference ranges. He notes that B12 norms were historically 300–1200 pg/mL but have been relaxed to as low as 170 pg/mL so patients ‘don’t worry.’ He counters that true physiological requirement is 600–1200. Similarly, homocysteine, a methylmalonic acid alternative, should be around 6–8 µmol/L, but labs now accept up to 20. He uses a personal anecdote from a gathering with Wiesław Brugo in Ostrów Mazowiecka where he saw attendees with homocysteine of 20 being told they were fine. He challenges: who is setting these norms, and who benefits? This twin test—B12 and homocysteine—thus becomes a tool not only for diagnosing deficiency but for exposing the gap between laboratory policy and biological reality. He ends by saying that if a doctor blindly trusts the lab range, they will miss the problem.

The speaker explains that D-dimer is a fibrin degradation product that rises when there is active clotting. He has previously dedicated an episode to superficial and deep vein thrombosis, and here he stresses that the test should be part of the basic annual panel. He claims that norms have been raised so that a value that used to be alarming is now considered normal, lulling patients and doctors into complacency. He states clearly: the real upper normal limit should be 300 (in units of ng/mL, or 0.3 depending on the lab). If D-dimer is elevated, it means something is coagulating silently, potentially leading to stroke or myocardial infarction. He therefore sees this as a screening tool for subclinical thrombosis.

The speaker describes it as a harmless, rapid test using spectrophotometry (the same principle as the spectrophotometers in all labs) and giving immediate results on excesses, deficiencies, and toxin locations. He notes that a complete diagnostic picture should include blood, urine, Sołczek, and possibly bioresonance or hair spectral analysis to see how the body is cleansing itself and what is blocking its detox mechanisms. The test is available in Poland.

The speaker delivers a passionate warning: classic endodontics declares dead teeth ‘fine,’ but under the crown, at the apex, low-oxygen conditions turn normally harmless bacteria virulent. Gram-negative anaerobes thrive, and if the culprit is Streptococcus viridans, it can travel to the heart and cause acute valve perforation. He references the systemic infection risk that many in mainstream dentistry ignore. The pantomogram must be read by someone who knows these connections; a biological dentist will spot early cystic lesions and recommend intervention before the bacteria spread. This test, he insists, belongs in the basic workup because it can prevent catastrophic events.

The speaker emphasizes that the enzyme responsible for the 1α-hydroxylation is present in the brain, pancreas, vascular endothelium, endocrine glands, gonads, breast tissue—anywhere there is high biological activity. Therefore, when 25-OH-D3 is low, multiple organs may be unable to produce sufficient active vitamin D locally, even if the serum 1,25-dihydroxy vitamin D level appears normal. This insight elevates the prohormone 25-OH-D3 as the true indicator of vitamin D status. He warns that the active form can be normal even in sick individuals, making it an unreliable test.

The speaker recounts a recent gathering where he saw patients with homocysteine of 20 µmol/L told they were fine. He mockingly asks 'Kto tworzy te normy?' (Who creates these norms?). For B12, he says the real healthy range is 600–1200 pg/mL; the lower limit of 170 or even 300 is absurd. For D-dimer, the true safe upper limit is 300 ng/mL, but labs now cite 500 or even 0.5 (depending on units). He warns that doctors relying on widened norms will miss early warning signs and fail to act, leaving people with silent risks.

The speaker explains that doing glucose and insulin not on an empty stomach but precisely one hour after eating can unmask insulin resistance: glucose may remain within range while insulin is already elevated. He also links this to a broader point about diagnostic sloppiness—many older adults are diagnosed with type 2 diabetes but actually have late-onset type 1, detectable with anti-GAD, anti-IA-2, and anti-ZnT8 antibodies. This suggests that even when diabetes is suspected, the standard workup is often incomplete.

The speaker details that at the apex of a root-treated tooth, cysts, inflammation, necrosis, and tissue softening often develop. These create oxygen-poor conditions where normally non-pathogenic bacteria turn aggressive. If it's Streptococcus viridans, the bacteria can travel to the heart and cause acute perforation of the valves—a life-threatening emergency. He therefore urges that a pantomogram must be analyzed by a biological dentist who understands this hidden focal infection threat, not by a regular dentist who may dismiss it.