Perspectives in Human Biology

The following sections are included:

• PREFACE

• CONTENTS

This paper looks at some questions which face policy makers and administrators who are required to make decisions about the interaction between government and its agencies and the Aboriginal people of Australia.

The published measurements of the social condition of Aborigines are uniformly regarded as indicating an unsatisfactory situation which demands remedial action by governments. My dealing with some of the issues is undoubtedly coloured by my experience. When, as a non-Aboriginal policy maker for Aborigines, you are told that it is because of you that such adverse social conditions persist, that is an imperative for intervention. The record of the post-Second World War period suggests that that imperative will remain with us, and that successive future governments will, like the governments of the past, struggle to find approaches which will produce outcomes deemed acceptable by Aborigines and non-Aborigines alike.

Because it seems so obviously irrational to have additional children when one lacks the resources to care adequately for the children one already has, the world's poor are often judged immature, immoral, or unintelligent, with dangerous consequences for their health and human rights. The goal of this paper is to refute this incorrect and damaging folk belief. The paper begins with a review of the ‘general life history problem’ in evolutionary ecology and the critical tradeoff between current and future reproductive success. Because natural selection ultimately favours adaptations for reproductive success - not health or life span - when people are denied access to power and other resources it may be (or have been) evolutionarily adaptive for them to behave in ways that are not necessarily conducive to health or long life. The paper concludes with a brief discussion of the implications of this argument for the emerging field of Darwinian medicine.

The Western Australian Birth Defects Registry was established in 1980, with the aims of delineating the frequency of birth defects; conducting research into their causes, treatment and prevention; investigating changes in patterns of birth defects; and providing information about birth defects to health professionals and the public. Information from the Registry has been used in genetic counselling; has assisted in identifying the need for a policy to vaccinate migrant women against rubella; has defined the magnitude of the problem of diabetes as a cause of birth defects in infants of Aboriginal women; has been used to investigate the role of chromosome 22q11 deletions in the aetiology of congenital heart disease; and has had a major role in research into folate and neural tube defects, from basic aetiological studies through professional and public education to primary prevention.

Retrospective demographic and ethnographic data collected on the South-Eastern Micronesian atoll of Butaritari are employed to test for factors affecting the differentials and patterning of post partum amenorrhoea in this well-nourished population. Of the covariates examined in a hazards model, mother's age at the birth of the child and cessation of breastfeeding failed to have any statistically significant effect on the duration of post partum amenorrhoea. Comparing these results with those for other ‘anthropological’ populations, we conclude that relatively rapid post partum returns of menses may be characteristic of Pacific Island populations. However, we propose that there is no evidence that patterns of post partum amenorrhoea in these ‘robust’ groups are expected in reference to breastfeeding variables. Rather, we suggest an interesting and important feature of these populations, as indicated by the Butaritari case, may be the lack of any maternal age effect on the resumption of menses post partum.

In the last quarter of the 20th Century there has been an unpredicted increase in survival of humans beyond the age of 80 years in developed countries. This phenomenon is attributed to the success of public health interventions for the chronic age-related systemic diseases, such as heart disease, stroke and cigarette-related lung disease and cancers. This increased survival of the very old (those over 80 years of age) will produce an increase in the prevalence of the neurodegenerative diseases (Alzheimer's disease, Parkinson's disease and cerebellar ataxia) all of which increase in prevalence with advanced age. We hypothesize that the age-related changes in neurological function seen in the old-old population are largely due to prodromal or early manifestations of the neurodegenerative diseases. Both the diseases and the age-related changes are associated with the clinical syndromes of dementia and confusion, immobility, gait disorder and falls, and incontinence which are major causes of loss of independence and need for institutional care.

At present there are no known modifiable environmental or socio-economic risk factors for the late onset neurodegenerative diseases and ‘brain ageing’ changes which will produce an age-related ‘epidemic’ in the first part of the twenty-first Century. We argue that a major search for possible environmental risk factors is essential. A successful outcome to such a search would lead to the delayed onset and hence reduced prevalence of both the neurodegenerative diseases and the syndrome of ‘brain ageing’, with a corresponding improvement in the quality of life of the old-old.

Historical and current approaches to extending life span are reviewed to show that average but not maximal human life span can be increased. In animals, calorie restriction extends maximal and average life span, and delays the onset of age-related conditions. Possible explanations are increased intracellular proteolysis, decreased circulatory glucose, decreased cellular proliferation rate, increased melatonin levels, or over-eating by control animals. Human cells in culture (lung fibroblasts) senesce and eventually cease dividing after a maximum of about 50 cell divisions (the Hayflick limit). Vitamins A, C and E do not increase the Hayflick limit but hydrocortisone, low doses of ionizing radiation and tumour suppressor gene anti-sense RNA do. Delay of fibroblast senescence and extension of Hayflick limit has been recently shown to occur in the presence of 20 and 30mM carnosine (β-alanyl-histidine) normally found in nervous tissues at concentrations up to 20mM. Previously suggested to be an anti-oxidant and free-radical scavenger, a buffer, metal ion chelator and neurotransmitter, intramuscular carnosine concentrations correlate with species maximal life span. Carnosine resembles preferred sites in proteins where sugar aldehydes attack (non-enzymic glycosylation or glycation) producing crosslinks.

We show that carnosine (i) is glycated by glucose and more reactive sugars and aldehydes; (ii) protects proteins (crystallin, serum albumin and anti-thrombin III) against cross linkage by acting as a sacrificial amino sink; (iii) protects cells (fibroblasts and lymphocytes) against acetaldehyde-induced death; (iv) can stimulate proteolysis in fibroblasts; (v) glycation products formed with glucose are not mutagenic (those produced by lysine or arginine and glucose are mutagenic). Hence carnosine possesses properties consistent with its anti-ageing action in cell cultures. It is not known whether carnosine has similar effects at the whole animal level. Carnosine is usually present in meat, is non-toxic and might be beneficial to humans. However, current advice, which advocates eating less meat, (because of its generally high saturated fatty acid content) may also result in a decreased intake of carnosine. We speculate whether carnosine or other unidentified anti-glycators might be beneficial in controlling ageing in general, and the development of secondary complications in diabetics.

In the majority of Middle Eastern countries, consanguineous marriages currently account for 20% to over 50% of all unions with no evidence to suggest a significant decline in their popularity. Consanguinity generally is associated with increased fertility, and mortality is higher among consanguineous progeny due to the expression of detrimental recessive genes. There also is evidence of greater morbidity in children born to consanguineous parents, which may extend into early and late adulthood. With improved primary health care, deaths and disability due to infectious diseases can be expected to decline in prevalence and genetic disorders will absorb an increasing proportion of the future health care budget in the region. Under such circumstances the burden of ill-health will fall disproportionately on communities in which consanguinity is strongly favoured. However, when assessing the overall effects of inbreeding, and to ensure that counselling programmes are devised to match the requirements of the population, it is important that the traditional social and economic benefits associated with marriage to a close relative are fully taken into consideration. It is suggested that there is an urgent need for prospective multi-disciplinary studies into the medical, biological and social consequences of consanguineous marriage with, as an interim measure, the formulation and introduction of training programmes for genetic counsellors recruited from local populations.

This study examines facial flatness in East/Southeast Asian and Australian Aboriginal samples to investigate inter-relationships in this area and their possible evolutionary implications. The major findings are as follows. (1) Australians and Melanesians are two branches of one major stem. (2) The simotic index representing the flatness of nasal bones tends to be independent of the frontal and zygomaxillary indices. (3) In the East/Southeast Asian and the near Oceanian region, there is a rough clinal variation of facial flatness from north to south. (4) Australian Aborigines together with Melanesians show the same degree of facial flatness as that of Europeans except for the nasal region. And (5), facial flatness may be an unstable trait in human evolution. Taking the fossil evidence such as Sangiran 17 Homo erectus and the terminal Pleistocene Wajak I as well as several Australian specimens into consideration, facial flatness may not be a character supporting the multiregional evolution hypothesis for the emergence of anatomically modern humans, at least in the East/Southeast Asian and Australian regions.

The following sections are included:

• BOOK REVIEW