1.
Big brains, meat, tuberculosis and the nicotinamide switches: co-evolutionary relationships with modern repercussions on longevity and disease?
Williams, AC, Dunbar, RI
Medical hypotheses. 2014;(1):79-87
Abstract
Meat eating has been an important trigger for human evolution however the responsible component in meat has not been clearly identified. Here we propose that the limiting factors for expanding brains and increasing longevity were the micronutrient nicotinamide (vitamin B3) and the metabolically related essential amino-acid, tryptophan. Meat offers significant sourcing challenges and lack causes a deficiency of nicotinamide and tryptophan and consequently the energy carrier nicotinamide adenine dinucleotide (NAD) that gets consumed in regulatory circuits important for survival, resulting in premature ageing, poor cognition and brain atrophy. If a trophic supply of dietary nicotinamide/tryptophan is so essential for building brains, constraining their size and connectivity, we hypothesise that back-up mechanisms to ensure the supply evolved. One strategy may be increasing the reliance on gut symbionts to break down celluloses that produces NADH and only nicotinamide indirectly, and may cause diarrhoea. We suggest that a direct supplier was the chronic mycobacterial infection tuberculosis (TB) that is a surprise candidate but it co-evolved early, does not inevitably cause disease (90-95% of those infected are healthy), and secretes (and is inhibited by) nicotinamide. We hypothesise that TB evolved first as a symbiont that enabled humans to cope with short-lived shortages of meat and only later behaved as a pathogen when the supply deteriorated chronically, for those in poverty. (TB immunology and epidemiology is riddled with paradoxes for a conventional pathogen). We test this in pilot data showing that sharp declines in TB (and diarrhoea) - `environmental enteropathy' strongly correlate with increasing meat consumption and therefore nicotinamide exposure, unlike later onset cancers and Parkinson's disease that increased in incidence, perhaps - as we propose a hypothetical hypervitaminosis B3 (to include obesity and the metabolic syndrome) - as the trade-off for increased brain power and longevity, a recently evolved human characteristic.
2.
[Correction of central nervous system energy processes in children with the minimal cerebral dysfunction].
Lavrik, SIu, Domitrak, SV, Shprakh, VV
Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova. 2011;(4):37-41
Abstract
Clinical-neurophysiological investigation of the efficiency of complex metabolic neuroprotector Cytoflavin in monotherapy was performed in 64 children of 4-8 years old with the minimal cerebral dysfunction. During the treatment other preparations were not used. Neurologic status, neurophysiological inspection, neuropsychophysiological and speech testing were performed before and after the course of treatment. Efficiency of Cytoflavin was established in children with the minimal cerebral dysfunction of preschool and early school age. By increasing a cerebral blood flow, improving parameters EEG and decreasing intracranial pressure, the drug had positive influence on the psycho-emotional and cognitive spheres, decreased asthenia syndrome, improving social adaptation of the children. Side-effects of Cytoflavin administration were not observed.