Boy Girl Ratios —
In Nature 2007, vol 450 p 765 there is a fascinating summary of two papers describing variations in male female ratios in babies
. Biol. Lett. doi:10.1O98/rsbl.2007.0482 (2007);
Proc. R. Soc. B doi:10.1098/rspb.2007.1401 (2007)
Evolutionary theory suggests that sexual creatures increase the number of descendants if they have more sons than daughters when conditions are optimal and more daughters than sons in less ideal circumstances. How this happens is not clear.
It may also be that after wars, more male babies are born than female.
Samuli Helle, of the University of Turku in Finland, and his colleagues report a correlation between the annual mean temperature in northern Finland and the sex ratio of newborns in three populations of indigenous Sami people for the years 1745-1890. The team compared demographic data from the parish registers of Lutheran churches with a climatic record reconstructed from tree rings and an index of the North Atlantic Oscillation. Warmer years brought an increased proportion of boys, in keeping with theory.
Elissa Cameron, of the University of Pretoria in South Africa, and her colleagues raised the proportion of daughters in mouse litters by lowering the blood glucose levels of females during conception. The researchers added dexamethasone, a steroid that blocks glucose uptake into the blood, to the drinking water of female mice for three days while the animals had access to a mate. Only 41,9% of the litters of dexamethasone-treated mice were male, compared with 53.5% in control litters.
This suggests a fascinating research project. The effect of diet on the male female ratio of offspring. Easy in mice. Firstly a nutritionally adequate , an adequate and insufficient diet.
Pregnancy can often happen if he girl is drunk so study alcohol ( beer, white and re wine )
Then the vast array of food and herb aphrodisiacs, which include oysters and chocolate.
Brain Development —
The mammalian central nervous system is a very complicated system, with an array of different cell types each with its singular morphology, connections and function. The phenotypic properties of each cell are the product of combinations of expressed gene products peculiar to that cell type. The Allen brain atlas project ( http://www.brain-map.org is studying the genetic structural and cellular architecture of the mouse brain. A mammoth undertaking using complex techniques. There are approximately 20,000 expressed genes in the adult mouse brain. The project looks at genes with regional expression patterns allowing descriptions for functional similarities across the 12 major brain regions.
Classical definitions of brain regions is based upon a combination of overall morphology, cellular cytoarchitecture, ontological development and functional connections. Such studies offer insights into brain structure and function, and may also challenge our definitions of brain structure which are anatomical and to an extent functional.
Lein et al 2007, Nature Jan 11, vol 445 pp 168-176
However these genes can only effectively express themselves if they have substrates to work with. The foetal brain grows rapidly during gestation ,weighs 350g (of which 50% is lipid ) at birth and triples in weight during the first two years of life. The lipids are predominantly polyunsaturated long chain fatty acids , some of which are essential fatty acids. These are derived from preformed fatty acids or precursors. Of the fatty acids docosahexaenoic and arachidonic acids are the most important. Much of which is obtained from the diet.
It would appear that eating fish results in better neurological development than when the mother has a poor or absent fish intake.
This raises two questions. Fish contain small amounts of unwanted contaminants e.g. methylmercury, and possible toxicity problems for the foetus.
And raises the irreverent thought, should Eskimos be the cleverest people on earth.
Lancet vol 369, February 17th, pp537-8 ; and Hibbeln et al Lancet , vol 369. pp 578-85
Flippancy apart this is very important observation
At the other end of life the brain begins to loose cognitive function, largely expressed as failing memory. The elderly with low serum folate and raised homocysteine concentrations are at risk of reduced cognitive function. In a large double blind randomised placebo controlled clinical trial in the Netherlands it was shown that taking 800 ųg of folic acid a day significantly improved cognitive memory. Again nutrition affecting a complex system.
Durga et al Lancet 2007, vol 369, pp 208-16
We Nutritionists live in a world which generates a fantastic array of scientific advances especially in molecular biology which appear to make nutrition less relevant. Perhaps we should see this as a great opportunity to clarify many of the mysteries of nutrition and health.
Huntington’s disease or Huntington’s chorea is a terrible dominantly inherited neurodegenerative disease. The basis of this problem is an accumulation of fragments of polyglutamine expanded protein in affected neurons. There is also in Huntington’s disease and Alzheimers an abnormal enrichment of ubiquitin. Ubiquitin metabolism may be in disarray. Ubiquitin is widely found in cells and nuclei and undergoes an ATP dependent reaction with proteins with condensation of its terminus with lysine amino groups. Cyclin degradation in the control of the cell cycle is triggered by ubiquitination .
Huntington’s disease is thought to be secondary to quite wide spread changes in ubiquitin metabolism.
Bennett et al 2007 Global changes to the ubiquitin system in Huntingdon’s disease.
Placenta and Vitamin A —
Vitamin A is vital during the initial stages of life. Important is embryonic development, tissue homeostasis, lipid metabolism and cellular differentiation and proliferation. Human placentae express factors for the nuclear transcription of retinoic acid receptors and retinoic X receptors. Modulation of these factors by retinoic acid modulates the expression of several genes such as: chorionic gonadotrophic bormone; placental lactogenic hormone; leptin; epidermal growth factor receptor; triiodothyronine; oestrogen; progester¬one; cortisol; aldosterone; testosterone; vitamin D; cholesterol; and fatty acids.
This study examines the association between vitamin A deficiency measured by maternal serum retinol concentration, umbilical cord and placental concentration of retinol and carotenoids. This allows a defining of placental values representative of deficiency.
Two hundred and sixty-two mothers and their newborn babies were measured.
No difference between averages of placental retinol and carotenoids was observed in the puerperal women regardless of the cut-off point used to define vitamin A deficiency.
In the newborn babies there was a decrease in placental retinol values in individuals with vitamin A deficiency when a 1•05 umol/l cut-off point was adopted.
The placental carotenoid average concentration was reduced
This study shows an association between the placental concentration of retinol and carotenoids with clinical vitamin A deficiency.
Gomes et al 2010. Placenta: a possible predictor of vitamin A deficiency . British J Nutrition. vol 103 pp1340-1344
Vitamin A in Neonates —
Andrew Prentice in the BMJ 20th March 2010 comments on a linked randomised controlled trial, where Benn and col¬leagues ( BMJ 20th March 2010 ) assess the effect of giving high dose vitamin A supplements to low birth weight neonates in Guinea¬-Bissau. They found no effect on infant mortality, although boys tended to benefit but a significantly harmful effect was seen on girls’ survival.
In 1983 it was reported that young Indonesian children with mild xerophthalmia, Bitot’s spots, and night blind¬ness, ie vitamin A deficiency-had a higher mortality rate . A subsequent randomised controlled trial of vitamin A supplementation showed an impressive benefit on mortality. A meta-analysis of large scale trials in Asia and Africa showed that this cheap and simple intervention reduces child mortality by 30% in countries with evidence of at least marginal vitamin A deficiency. The World Health Organization recommended universal vitamin A supplementation of chil¬dren aged six to 60 months, which is government policy in more than 60 countries.
The question was than asked if it was better to give vitamin A to newborn babies or later to infants or children. Infant mortality is greatest in the first six months of life. Clinical trials of supplementing breast feeding mothers postpartum gave varying results and some infant complications eg acute bulging fontanelles after dosing. More trials were conducted and a meta-analysis found a mixed picture , no survival benefit, but evidence of benefit from Asian trials and evidence of no effect (or even harm) in two African trials eg previous one by Benn and colleagues in Guinea-Bissau.’
Yet vitamin A supplementation has saved many thousands of lives. Benn has indicated no benefit and even harmful effect of vitamin A at birth that seemed to be confined to girls. Benn has shown repeated examples of how vaccines, micronutrients, and exposure to infections can strongly affect all cause mortality in regions with a high burden of infection. Sex differences in susceptibility to certain infections and in responses to vaccination have been recognised for decades,
WHO has commissioned three large trials in an attempt to resolve the possibility that neonatal vitamin A supplementation may be beneficial in Asia but not in Africa. These trials will assess mortality up to six months of age.
Prentice 2010 Vitamin A supplements and survival in children BMJ vol 340 pp 607-8
Benn et al 2010 Vitamin A supplementation and BCG vaccination at birth in two low birthweight neonates: two by two factorial randomised trial BMJ vol 340 p 636