Aivojen lipidiaineitten turn over

About brain lipid turnover

August 25, 2011

It is very interesting how quickly the normal brain changes its lipids. lipid turnover was described already tens of years ago in the book of Harold A. Harper:

On kiinnostavaa, miten nopeasti normaali aivo uudistaa lipideitään, rasva-aineitaan. Tämä lipidien turn over tapahtuma oli kuvattu jo 1969 aikaan Harperin kirjassa seuraavasti.

The rate at which the lipids of brain are exchanged is relatively slow in comparison to that in an active organ such as the liver. Tracer studies with deuterium indicate that while 50% of the liver fats may be exchanged in 24 hours, only 20% of the brain fat is replaced in seven days.

Se tahti, millä aivojen lipidit vaihtuvat on suhteellisesti hitaampi verrattuna metabolisesti aktiiveihin elimiin kuten maksaan. Hivenainetutkimukset raskaalla vedyllä (D2) viittaavat siihen, että maksan uudistaessa vuorokaudessa ehkä 50 % lipideistään aivot uudistavat 20% lipideistään seitsemässä päivässä.

(Side 522 Nerve Tissue, The Lipids of Nerve Tissue, Chapter 22. The Chemistry of the Tissues, In: Review of Physiological Chemistry, 12th ed. 1969).

• Mitä tämä merkitsee nykyaikana, kun rasvaliukoisia aineita (alkoholia ja kannabista) käytetäänyhä suuremmassa väestönosassa? Sen kaltaiset molekyylit vaikuttavat häiritsevästi aivojen uusien rasvamolekyylien prosessoitumiseen ja paikoilleen asettumiseen. Ihmiskunnassa aivojen normaalirakenne muuntuu. Mitä sa vaikuttaa globaaliin genomiin ja globaaliin intelligenssiin? Eihän mainittujen aineiden haittavaikutukssa yleensä puhuta muusta kuin akuuteista ja hieman pitempiaikaisista haitoista ja sitten niitä ilmiselviä haittoja vertaillaan, vähätellään, eikä asialle antautuneitten intelligenssin muuntumisen takia pystytä näkemään globaalin aivon haittoja.
• Ehkä pitkäaikaiset kohorttitutkimukset aivoston muuntumisista joukoissa (PAD) voi antaa heijastusta siihen, mikä on globaalin aivon ja intelligenssin muutos orgaanisten ja lipidiliukoisten aineitten väärinkäytön ja käytön takia ihmiskunnassa. Kyseessähän on aivojen geneettinen muutos myös, apoptoosiprosessiin vaikuttaminen.
• ( Eivät kaikki ole MS potilaita, joilla tulisi pysäyttää nopea aivotulehdus ja säästää siten mitä on jäljellä, koska uusiutumista ja normaalia turn overia ei ole pystytty saamaan aikaan nykykeinoin. Ei kaikki ole aivosyöpäpotilaitakaan, joilla koetetaan jarruttaa jotain aivosolukasvua).
  

In our days (2011), the usage and especially the misusage of molecules ( alcohol, cannabis, other drugs) which intervene the replacing processof a new brain lipid, is escalating in a large part of population of the world. Misusage of lipid soluble molecules as alcohol and cannabis has an effect on brain metabolism and they cause a disturbance in the brain lipid turnover, and thus a relative change in the composition of the human brain in populations. Who knows what that means to the global genome and to the global intelligence, because the altered velocity of lipid exchange is not questioned at all among the indicators of brain damages and functional impairments of kognition. People talk only about e.g. acute toxicity and compare acute damages of alcohol and cannabis. But all brains of misusers have changed or are changing there lipid turnover to an unnormal or altered level. Only PAD of the brains of cohorts can reveal the damage to the mankind.

The scientists are worried because they can not convince people about these alterations of intelligence and also about the basic prerequisites of bewared high kognitive capacities in the mankind. A basic prerequisite of a healthy brain is a normal tunr over of brain lipids. That is going on every day all the time, without any days of misusage of organic solvents and lipid soluble hazardous molecules hopefully. Always is a good thing to stop using such molecules, becaus the brain has its inborn normal capability to process new lipids and it is making its turn overs always.

Every day of teetotaling, sobriety, or even abstinence is a good thing for the living brain.

The normal food is its best medicine.

Search: lipid turnover in brain

PubMed article:

Med Hypotheses. 2011 Aug 20. [Epub ahead of print]
Augmentation of chemotherapy-triggered glioma cell apoptosis by blockade of arachidonic acid metabolism-the potential role of ceramide accumulation.
Omahen DA.
Abstract

There has been recent interest in using cyclooxygenase-2 inhibitors in an effort to increase the efficacy of chemotherapy and/or radiation for treatment of malignant brain tumors. Although the mechanism is unclear, one result may be the accumulation of arachidonic acid (AA). AA is the key substrate for several biochemical pathways involved in the inflammatory cascade, including the cyclooxygenase (COX) enzymes. Cyclooxygenase-1 and cyclooxygenase-2 metabolize AA to produce prostaglandins and thromboxanes. Levels of these enzymes and their products are upregulated in gliomas, especially in malignant tumors. Likewise, the enzyme 5-lipoxygenase, also elevated in malignant gliomas, metabolizes AA to produce leukotrienes. Alternatively, enzymes of the cytochrome p450 family can metabolize AA to various products, some of which may aid glioma growth and angiogenesis. Unmetabolized AA activates the enzyme neutral sphingomyelinase, which produces ceramide, a second messenger and potent activator of apoptosis. It is hypothesized that simultaneous blockade of the COX, lipoxygenase, and/or cytochrome p450-mediated pathways would lead to greater accumulation of intracellular AA, resulting in elevated ceramide levels, thereby priming glioma cells for treatment-induced apoptotic cell death. Manipulation of AA/bioactive lipid metabolism, using readily available, well-tolerated medications may have the potential to increase the efficacy of currently used glioma treatments.

PMID:
21862232
[PubMed - as supplied by publisher]