PubMed Health⌕ Search

Biomedical subjects

L F Saugstad

Publications and source records attributed to L F Saugstad.

At least 19 recordsLinked to original sources
PubMed2001

Manic depressive psychosis and schizophrenia are neurological disorders at the extremes of CNS maturation and nutritional disorders associated with a deficit in marine fat.

The maturational theory of brain development comprises manic depressive psychosis and schizophrenia. It holds that the disorders are part of human diversity in growth and maturation, which explains their ubiquity, shared susceptibility genes and multifactorial inheritance. Rate of maturation and age at puberty are the genotype; the disorders are localized at the extremes with normality in between. This is based on the association between onset of puberty and the final regressive event, with pruning of 40% of excitatory synapses leaving the inhibitory ones fairly unchanged. This makes excitability, a fundamental property of nervous tissue, a distinguishing factor: the earlier puberty, the greater excitability--the later puberty, the greater deficit. Biological treatment supports deviation from the norm: neuroleptics are convulsant; antidepressives are anti-epiletogenic. There is an association between onset of puberty and body-build: early maturers are pyknic broad-built, late ones linearly leptosomic. This discrepancy is similar to that in the two disorders, supporting the theory that body-build is the phenotype. Standard of living is the environmental factor, which affects pubertal age and shifts the panorama of mental illness accordingly. Unnatural death has increased with antipsychotics. Other treatment is needed. PUFA deficit has been observed in RBC in both disorders and striking improvements with addition of minor amounts of PUFA. This supports that dietary deficit might cause psychotic development and that prevention is possible. Other neurological disorders also profit from PUFA, underlining a general deficit in the diet.

Biological Evolution↗
PubMed1999

A lack of cerebral lateralization in schizophrenia is within the normal variation in brain maturation but indicates late, slow maturation.

The planum temporale (PT) bias, PT leftward, PT symmetry, and PT rightward reversal and sidedness preference, consistent right-handedness, ambilaterality, and consistent left-handedness are placed on a continuum mirroring the normal variation in rate of brain maturation. Maturational rate declines as we pass from PT leftward bias and consistent right-handedness to PT reversal and consistent left-handedness. Concomitantly, we expect an increased prevalence of males due to their pubertal age being about 2 years later than that of females, and a shift in cognitive profile from higher verbal scores than performance scores on the WAIS to higher performance than verbal scores. Three disorders fulfilling the criteria of late CNS maturation apart from the corresponding cognitive profile were studied: infantile autism (IA), schizophrenia (S), and developmental dyslexia (DD). These disorders have in common deficits in cognition, perception, and somatomotor function. The deficits range from an arrest in brain development (which is evident in infancy superimposed on late maturation in IA) to overall delayed brain and somatic development in S (culminating in postpubertal psychotic episodes and persistent and generalized residual deficits). Finally, reading inability, problems in perception (vision and hearing) and in motor coordination, particularly between the two hemispheres, characterize DD. Enhancing brain maturation and the prevalence of 'normal' cerebral asymmetry--laterality is preferable if we want to reduce the risk of developing the above-mentioned disorders. It is suggested that in the past environmental challenges have favored early maturation, with its abundant neuronal population, arborization and excessive density of synapses and cerebral excitability which has powered evolution through the mechanism of natural selection. Early maturation is obtainable through optimal nutrition, including a satisfactory amount of marine fat (PUFA), before and during pregnancy and later in life.

Autistic Disorder↗
PubMed1999

Optimality of the birth population reduces learning and behaviour disorders and sudden infant death after the first month.

The weight distribution pattern of all births can be divided into a "skewing to the left" to lower weights and high neonatal mortality, a "skewing to the right" to higher weights (>3500g) and minimum neonatal and postneonatal mortality, and a "symmetrical distribution" with mortality in between. This study was initiated with the hypothesis that a deficit in newborns of more than 3500 g would adversely affect postneonatal death. Higher and rising postneonatal mortality solely attributable to sudden infant death of unknown cause (sudden infant death syndrome; SIDS) was observed in the Nordic countries with a lower proportion of heavy newborns. Minor environmental intervention almost eliminated excess mortality from this cause, supporting raised susceptibility with a depressed birthweight in postneonatal SIDS. This contrasts with classical neonatal low birthweight SIDS, which is stable despite numerous attempts at reduction, supporting a multi-factorial aetiology: low maternal age, low education, low socioeconomic status, maternal smoking, infection, etc. The postneonatal SIDS epidemic associated with a deficit in heavy newborns is thought to be a result of changing behaviour in pregnancy: moderate iatrogenic dietary restriction and young women favouring a low-calorie, low-fat diet, especially in the third trimester when the foetus is most vulnerable, which delays myelination and somatic growth and renders the infant susceptible to minor morbidity and irregularity. The timing of death and neuropathological findings suggestive of repeated hypoxic episodes in more than 80% of cases of SIDS prior to death support this theory. The similar weight distribution patterns in SIDS and all births in Denmark, the UK and the USA suggest a substantial proportion of the neonates in these countries could be growth-retarded and at risk of hypoxic episodes in infancy. A few cases, particularly males (sex-ratio = 1.7), suffer SIDS, the majority survive. Many, mostly males, present minor CNS signs and learning and behaviour problems. The male predominance accords with males more than 500 g higher optimal birthweight than females and susceptibility to a depressed weight at birth. In order to prevent postneonatal dying, SIDS and reduce learning/behaviour disorders it is necessary to raise the proportion of heavy newborns by promoting foetal growth rate equal to the maternal intrinsic rate by eating to one's appetite a balanced diet, favouring a diet high in marine fat, especially in third trimester, in order to ensure maturation of the CNS and prolong gestation, thereby increasing birthweight. Although the increased survival of some very low birthweight neonates confounds the issue, a division between SIDS in neonatal and postneonatal death is recommended in order to assess the proportion of "avoidable infant death" as opposed to persistent classical neonatal SIDS.

Birth Weight↗
PubMed1998

Cerebral lateralisation and rate of maturation.

Multifactorial inheritance applied to brain development implies a large continuum of normal variation with deviation from the norm at the extremes of maturational rate. The greater population of neurons, greater arborization of neural networks and excessive synaptic density in early maturation imply that adaptability (plasticity) is a main advantage, as opposed to a deficit in adaptability associated with the reduced number of neurons, reduced connectivity and reduced synaptic density in late slow maturation. It is hypothesised that Planum Temporale (PT) asymmetry and hand-preference predict the rate of CNS maturation as does the cognitive profile on the Wechsler Adult Intelligence Scale (WAIS): PT leftward asymmetry, right-handedness and a left-hemisphere cognitive advantage signifies early fast maturation: PT rightward asymmetry, left-handedness and a right-hemisphere cognitive advantage signify late maturation, while PT symmetry and ambilaterality represent rates of maturation in between. The slower development of males implies a male predominance in disorders affecting late maturers: Developmental Dyslexia (DD) with a predominance of rightward PT asymmetry/symmetry, left-handedness and multiple functional deficits, as well as excessive regressive events confirmed on PT/MRI. Schizophrenia, hypothesised to be a disorder in late maturers, is distinguished by rightward asymmetry/symmetry. Left-handedness and DD are common as is prior delayed development supporting excessive regressive events as do the findings on PT/MRI. To reduce the risk of DD and schizophrenia requires a reduction in late maturation through the enhancement of maturational rate by optimal nutrition before and during pregnancy and later.

Adult↗
PubMed1997

Optimal foetal growth in the reduction of learning and behaviour disorder and prevention of sudden infant death (SIDS) after the first month.

A theory is presented that a diet low in polyunsaturated fatty acids (PUFA) in the third trimester of pregnancy may delay myelination and brain maturation. This may underpin learning and behaviour disorders and sudden infant death (SIDS) after the first month, conditions that are associated with lower than average birthweight. Epidemiological evidence is reviewed showing an inverse relation between the proportion of heavy newborns (> 3500 g) and infant mortality rate. Some countries with a lower proportion of heavy newborns despite equally high standards of living and medical care have higher post-neonatal death rates. The higher rates are solely due to SIDS which has a peak mortality within 80-100 days. It is hypothesised that as this is a time when myelination peaks, SIDS may be due to maturational delay. Evidence of subtle CNS changes in brainstem structures and in the neuromuscular system supports an instability in brainstem control systems. Moderate iatrogenic dietary restriction predominates today, but a rising number of women favour a low-caloric low-fat diet especially in the third trimester when the foetus is most susceptible. This may lead to a depressed birthweight, delayed somatic growth and neuronal maturation, such as is observed in SIDS victims. The majority exposed to suboptimal conditions survive, but a few suffer SIDS; confirming post-neonatal susceptibility. Many, especially males, present minor CNS signs and learning/behaviour disorders that could be the sequelae of repeated hypoxic episodes, such as recorded in more than 80% of SIDS victims. To reduce learning/behaviour disorders and prevent death from SIDS after the first month, it is necessary to ensure optimal development by promoting foetal growth. It is advised to avoid unnecessary dieting and to favour a diet high in PUFAs, thus prolonging pregnancy and so increasing birthweight.

Birth Weight↗
PubMed1994

The maturational theory of brain development and cerebral excitability in the multifactorially inherited manic-depressive psychosis and schizophrenia.

An association has been established between the multifactorially inherited rate of physical maturation and the final step in brain development, when some 40% of synapses are eliminated. This may imply that similarly to endocrine disease entities, we have cerebral disease entities at the extremes of the maturational rate continuum. The restriction of prepubertal pruning to excitatory synapses leaving the number of inhibitory ones fairly constant, implies changes in cerebral excitability as a function of rate of maturation (age at puberty). In early maturation there will be an excess in excitatory drive due to prematurely abridged pruning, which compounds a synchronization tendency inherent in excessive synaptic density. Lowering excitatory level with antiepileptics is hypothesized to be a logical treatment in this type of brain dysfunction. In late maturation, a deficit in excitatory drive due to failure to shut down the pruning process associated with a tendency to the breakdown of circuitry and desynchronization, adds to a similar adversity inherent in reduced synaptic density. Raising the excitatory level with convulsants is hypothesized to be the treatment for this type of CNS dysfunction. The maturational theory of Kraepelin's psychoses holds that they are naturally occurring contrasting chemical signaling disorders in the brain at the extremes of the maturational rate continuum: manic depressive psychosis is a disorder of the early maturer and comprises raised cerebral excitability and a raised density of synapses. This is successfully treated with anti-epileptics like sodium valproate and carbamazepin. Schizophrenia is a disorder in late maturation with reduced cerebral excitability and reduced synaptic density. This is accordingly treated with convulsants such as typical and atypical neuroleptics. However, the conventional effective treatments in both disorders act on inhibition only by either lowering or raising inhibitory level. While the neuroleptics drugs are superior anti-psychotics they nevertheless do not affect the deviation in cerebral excitability which would explain why they do not cure. Disturbed circadian rhythms which precede psychotic episodes in manic depressives accord with a primary dysfunction in the CNS, the suprachiasmatic nucleus of the hypothalamus via its direct input the glutamatergic retinohypothalamic tract. The residual deficits in schizophrenia accord with persistently disconnected circuitry and communication which is a consequence of reduced excitatory level and is manifested in insufficient motivation, a reduced drive associated hypofunction, and neuromuscular dysfunction.

Bipolar Disorder↗
PubMed1994

Deviation in cerebral excitability: possible clinical implications.

Schizophrenia, a chemical signaling disorder in the brain, is also a deteriorating neurological disorder. The deficit in cerebral excitability, and associated reduced synaptic density, imply a risk of cortical breakdown of circuitry accompanied by an insufficient fill-in mechanism, and persistent silent spots, but no total loss of function, only dysfunction. This is subjectively experienced as deficiencies of cognition, perception and sensorimotor phenomena depending upon localization and connections of the disconnected circuitry. Considering the adversity inherent in this neural network, both the fast Hebbian pre-post form of learning and the slow pre-modulatory coincidence form of learning are probably impaired. The use of Feed Back Loops which usually govern our behaviour might also be impaired. In addition, we have to consider the daily problem of insufficient drive and motivation. Manic depressive psychosis, a chemical signaling disorder in the brain, is a true functional psychosis. The raised excitatory drive and raised synaptic density imply raised risk of uncoupling of circadian rhythms via the direct glutamatergic input to the suprachiasmatic nucleus of hypothalamus (SCN). This episodic brain stem dysfunction illustrates how a deficit in inhibition renders the brain unstable. The requirements of the fast Hebbian form of learning should easily be met, and neither should the slow forms of learning present a problem in networks characterized by excessive density.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral Cortex↗
PubMed1991

Persistent pelvic pain and pelvic joint instability.

As accepted as the condition of pelvic pain and pelvic joint instability (PPPJI) is in pregnancy, as controversial and doubted is the same diagnosis in non-pregnant women. Women suffering severe incapacitating PPPJI for years following parturition have recently founded an association. This offers a unique opportunity to investigate their characteristics. 153 of the 215 members answered a questionnaire. The majority (110) suffered PPPJI in first pregnancy with onset preceding 20 weeks gestation in 84 women. Onset was significantly earlier in users of oral contraceptives than in non-users (16.3 weeks and 20.5 weeks, respectively). The 153 women did not differ from the controls with regard to life-style, diseases prior to reproduction or reproduction. Their 358 deliveries were characterized by a marked excess of post-term deliveries, a raised proportion of infants of 4000 g or more, an extremely low sex-ratio of offspring (0.84) with 54.5% female births, and a significantly raised congenital hip dysplasia rate, consistent with elevated oestrogen and relaxin levels.

Birth Weight↗
PubMed1991

Is persistent pelvic pain and pelvic joint instability associated with early menarche and with oral contraceptives?

A study of 153 women with persistent pelvic pain and pelvic joint instability (PPPJI) following parturition, revealed that the women differed from the controls by a significantly lower age at menarche. Precocious puberty is associated with a fibrous dysplasia which resembles that seen in some PPPJI women patients at operations. Precocious puberty is known to be associated with hypothalamic dysfunction. Following cessation of lactation, 70 of 153 women did suffer galactorrhea and breast discomfort, suggesting a possible affection of the hypothalamic-pituitary system. Age at menarche was higher in users of oral contraceptives (OC) than in non-users, but onset of PPPJI was significantly earlier by gestation, and galactorrhea, and breast discomfort more frequent (60% affected as compared to 30% of non-users), suggesting that use of OC affects the hypothalamus in a manner similar to that associated with very early puberty. The widespread use of contraceptives is important if it truly leads to an increased proportion of PPPJI among reproducing women. Onset of puberty, controlled by the hypothalamus, coincides with the final step in brain development--elimination of some 40% of neuronal synapses. Age at puberty has declined by some 4 years in 100 years, and it is still falling. It cannot be excluded that in some very early maturers, redundancy of neuronal synapses persists, and that this is associated with hypothalamic dysfunction.

Adult↗
PubMed1989

Social class, marriage, and fertility in schizophrenia.

The hypothesis is presented that the etiology of schizophrenia is neurodevelopmental: schizophrenia is a disorder occurring in extremely late maturers, whereas manic-depressive psychosis affects early maturers. This hypothesis is related to recent neurobiological findings and also to the following epidemiological and demographic topics covered by the author in her review of social class, marriage, and fertility in schizophrenia: Kretschmer's observations of body type differences between patients with schizophrenia and manic-depressive psychosis; trends in the incidence of schizophrenia and manic-depressive psychosis in industrialized versus developing economies; changing epidemiology of the subtypes of schizophrenia and of manic-depressive psychosis; sex differences in manic-depressive psychosis and schizophrenia; fertility and childlessness in schizophrenia; selection for marriage in schizophrenia; marriage patterns, inbreeding, and schizophrenia; social class, social mobility, and occupation in schizophrenia; social mobility and social selection; excess of schizophrenia in the lowest strata of society; social class, course, and outcome; and social stress and schizophrenia.

Bipolar Disorder↗
PubMed1989

Mental illness and cognition in relation to age at puberty: a hypothesis.

Onset of puberty is usually considered to coincide with the last major step in brain development: the elimination of some 40% of neuronal synapses. Mean pubertal age has declined by some 4 years during the last 100 years. There is a relation between age at puberty and body build, and between body build and mental illness. The difference in body build between schizophrenia (S) and manic-depressive psychosis (MDP) is similar to that between late and early maturers. It is suggested that S affects late-maturing individuals and MDP very early maturers. The observed marked rise in MDP and decline in the most malignant forms of S (non-paranoid) are in agreement with MDP and S as neurodevelopmental disorders occurring at the extremes of maturation. Maturational irregularities are most likely to occur at the extremes, and it is suggested that abbreviation of the regressive process may have led to persistent redundancy of neuronal synapses in MDP and that prolongation of the process past the optimal has yielded an inadequate synaptic density in S. The lack of cerebral abnormality in the majority of MDP and the presence of only subtle structural deficits in S, are in agreement with this. The two disorders are probably as old as mankind, and early puberty is the necessary factor for the development of MDP and late puberty is the necessary factor for that of S. There is an inverse relation between spatial ability and rate of maturation, whereas verbal ability is unaffected by maturational rate. From a previous predominance in both sexes, spatial ability (Performance IQ scores) has been reduced to below verbal ability (Verbal IQ scores) in the female sex and in early maturing males.

Aging↗
PubMed1989

Age at puberty and mental illness. Towards a neurodevelopmental aetiology of Kraepelin's endogenous psychoses.

The hypothesis of a neurodevelopmental aetiology of manic-depressive psychosis and schizophrenia is based on the relation between onset of puberty and the final regressive events in the central nervous system (elimination of 40% of neuronal synapses), and the discrepancy in body build in the two disorders which is similar to that between early- and late-maturing individuals. The marked rise in manic-depressive psychoses and decline in schizophrenia, particularly the non-paranoid categories, accompanying the decline in mean pubertal age by some four years during the past hundred years are taken as evidence that manic-depressive psychosis affects early maturers and schizophrenia particularly affects late maturers. Gender differences and social differentials accord with this theory. Redundancy of neuronal synapses characterises manic-depressive psychosis, and reduced density of synapses is a characteristic of schizophrenia, whereas 'normality', with optimal synaptic density, is in between.

Age Factors↗
PubMed1983

Persistent discrepancy in international diagnostic practice since 1970.

National admission statistics by diagnosis since 1970, were available from seven WHO member countries. All had officially introduced the ICD 8, but only two countries strictly adhered to the ICD categories in practice. The new 3-digit category 298 (Other psychosis) has met with no success, nor did the new subgroups of schizophrenia with a favourable outcome (295.4, 295.5 and 295.7) gain much acceptance. The discrepancy in diagnostic distribution is virtually unchanged from that before 1970 with a persistent wide concept of schizophrenia in U.S.A. and of depressive illness in England. A new feature is the striking increase in non-psychotic admissions at a time when there is a marked decline in the hospital population. This is taken to indicate that the social stigma attached to the term psychosis persists, and is met with evasion. A preference for unspecified terms (fourth digit 9) is evident, as is the use of terms which leave open whether the patient is psychotic or not (311 in ICD 9). Evidently, instruction in the use of the WHO glossary is called for. In the U.S.A. the replacement of the ICD by the local classification DSM-III is likely to accelerate the reluctance to accept international standards. Moreover, the development of local diagnostic systems for research purposes in England and U.S.A. is not without problems, as there is a disturbing lack of consensus in diagnosis between these two national systems. Obviously, we need the ICD with its clear concepts, and above all the ICD is valuable for securing continuity in diagnostic classification.

Bipolar Disorder↗
PubMed1981

Weight of all births and infant mortality.

Birth weight is the most important determinant of perinatal and infant mortality. The lowest mortality rates in the first week of life are recorded among newborn infants weighing 3500 g or more and the proportion of such infants may be regarded as a measure of optimality of the birth population. There is an inverse relationship between the proportion of heavy newborn infants in a country and its infant mortality rate. In both these respects Iceland, Norway, and Sweden have better experience than England and Wales, Denmark, and the United States of America. The effects of parity, maternal age, social class, and smoking are considered, but it appears that there are still factors that inhibit the intrauterine growth potential of American, British, and Danish fetuses. Elective delivery, use of diuretics, and restriction of diet in pregnancy have shifted the birth distribution to the left and this may have more than counterbalanced the possible beneficial effects. These other factors may adversely affect birthweight distribution in North America and Europe to such an extent as to limit or even damage the favourable position already achieved in health and social development as measured by fetal survival.

Birth Weight↗
PubMed1979

Mortality in psychiatric hospitals in Norway 1950--74.

The present investigation comprises all deaths in Norwegian psychiatric hospitals 1950--74: 10,413 deaths. Mortality in men declined from 361 per 10,000 before 1950 to 252 per 10,000 in 1969--74 and in women from 324 per 10,000 to 215 per 10,000 during the same periods. In the organic and symptomatic psychoses (mainly senile and arteriosclerotic) mortality ranged from six to ten times that of the general population, whereas in the non-organic (functional) psychoses mortality was only twice as high as in the general population. This discrepancy in mortality between organic and non-organic psychoses, which is caused by the somatic disorders with high lethality underlying the organic psychoses, suggests that mortality should be calculated separately for organic and non-organic psychoses, which is sometimes neglected. An increasing number of hospital admissions with organic, mainly senile, psychoses is to be expected in the future, as well as an increasing proportion of non-organic patients with slight psychotic symptoms and a low and possibly decreasing mortality. between 1950 and 1974 radical changes took place in the psychiatric hospitals which could have influenced mortality. Age-adjusted death rates from cardio-vascular diseases were actually higher in 1963--68 than in 1950--62, possibly indicating that an adverse effect of drug therapy on physical activity and somatic fitness had outweighed the stress-relieving effect. A significant rise in unnatural deaths (suicides and accidents) has been observed particularly since 1963. As in previous investigations from Norway 1926--41, cancer as cause of death was equal to or below the general population in the non-organic psychoses and somewhat higher in the organic psychoses.

Accidents↗
PubMed1977

The relationship between inbreeding, migration and population density in Norway.

An investigation of the present levels of inbreeding and the proportion of non-migrants (residents in municipality of birth) in rural districts of Norway reveals a relationship between these two characteristics. There is a steady upward trend from 0.39% first- and second-cousin marriages in municipalities with less than 50% non-migrants to 4.3% such consanguineous matings in municipalities where 85% or more of the inhabitants are non-migrants. There is also a significant negative correlation (rs=-0.86, N=18) between inbreeding and population density per square km by county in Norway. In rural districts of Norway maximum inbreeding is observed in sparsley populated areas with maximum proportion of non-migrants, and the ratio of second- to first-cousin marriages ranges between 3.4 and 4.1. A similar high ratio (3.7) is also encountered in densely populated trading and industrial municipalities and in the smaller towns, whereas the semi-urban municipalities and the larger towns have the lowest inbreeding recorded and also a low ratio (1.9). The lowest proportion of non-migrants (39.3%) is recorded in the semi-urban municipalities.

Consanguinity↗