Academic literature on the topic 'Locust response to diet change'

Context Despite the regular use of pesticides to control locusts, there is a lack of information on the effects of locust-control treatments on reptiles worldwide. Exposure to pesticides poses a significant potential hazard to small reptiles, both from the direct effects of exposure, and indirectly because of their largely insectivorous diet and small home ranges. Aims Our study aimed to monitor the effects of two insecticides applied operationally for locust control in Australia. A phenyl pyrazole pesticide, fipronil, and a fungal biopesticide, Metarhizium acridium (Green Guard®), were applied aerially in either a barrier or block treatment in the absence of dense locust populations, and effects on non-target arid-zone reptiles were measured. Methods We monitored reptile-abundance and community-composition responses to treatments using a large field-based pitfall-trapping experiment, with replicated control and spraying treatments, which approximated the scale of aerial-based locust-control operations in Australia. Key results Neither reptile abundance nor community composition was significantly affected by locust-control treatments. However, both abundance and community composition as detected by pitfall trapping changed over time, in both control and treatment plots, possibly as a result of a decrease in annual rainfall. Conclusions The absence of any significant short-term pesticide treatment effects in our study suggests that the two locust-control application methods studied present a relatively insignificant hazard to reptiles at our site, based on a single application. Similar to other areas of Australia, climate and other factors are likely to be stronger drivers of reptile abundance and community structure. Implications Monitoring over an area that approximates the scale of the current locust-control operations is an important step in understanding the possible effects of current pesticide exposure on reptile populations and will inform insecticide risk assessments in Australia. However, important information on the immediate response of individuals to insecticide application and long-term effects of exposure are missing. The preliminary research reported in the present paper should be complemented by future investigations on long-term and sublethal impacts of pesticide exposure on Australian native reptiles and the possible benefits provided to reptiles by the resource pulses represented in untreated high-density locust populations.

Two hundred and twenty five, day-old Arbour Acre broiler birds were use to investigate the effect of graded dietary levels of Parkia biglobosa pulp meal (PBPM) on the performance, haematological and carcass parameters of the birds from 0-8 weeks of age. Five isocaloric and isonitrogenous diets were formulated to contain PBPM at 0,10,20, 30 and 40 percent respectively making a total of 5 treatments. Each treatment was replicated three times with 15 birds per replicate in a completely randomized design experiment. Feed and water were supplied ad libitum. Records taken included weekly weight changes and weekly feed intake. There was no record of mortality throughout the duration of the experiment. Results obtained showed a decrease in the bird’s performance as the dietary levels of the pulp increased. The final weight (g/b) and weight gain (g/b/day) decreased from 2122 and 33.91 for the control to1309 and 20.97 for the 40% inclusion level of PBPM meal respectively However birds placed on 10% dietary level had a performance that were not significantly (P>0.05) different from those placed on the control diet which were on standard broiler starter and finisher rations. Also it was observed that values obtained for the haematological parameters fall within the range often reported for healthy birds indicating that the pulp did not impart any deleterious effect on the health of the birds. It can be concluded that broiler chickens can be fed up to 10% dietary level of PBPM without adverse effect on the performance of the birds.

1. Previous work has demonstrated that fifth-instar nymphs of Locusta migratoria L. respond to differences in levels of dietary protein by altering intermeal interval but not meal size (Simpson & Abisgold, 1985): insects fed a diet with 14% protein (p) eat the same sized meals more frequently than those fed a diet with 28% protein (P). The physiological basis for this compensatory response is investigated. 2. Insects fed the P-diet had a significantly larger increase in blood osmolality during and after a meal than did those fed the p-diet. 3. Unexpectedly, this difference in blood osmolality did not result in a variation in the rate at which the fore-, mid- and hindgut emptied. Therefore a change in the rate of decline in negative feedback from gut stretch receptors does not underlie the alteration in interfeed interval. 4. 40% of the difference in blood osmolality between p- and P-fed insects was attributable to changes in the blood concentration of free amino acids. Of the 16 free amino acids found, 11 occurred in significantly higher concentrations in the blood of P-fed insects. 5. There was no significant difference in the polypeptide and protein content of the blood of insects fed the p- or P-diet. 6. Increasing either blood osmolality or free amino acid concentration by injection delayed the next meal:injections that increased both had the greatest effect. 7. A mechanism is discussed whereby both blood osmolality and the concentration of various free amino acids regulate the time between meals, and thus compensatory feeding in response to changes in dietary protein.

The enzyme β,β-carotene-15,15′-mono-oxygenase 1 (BCMO1) is responsible for the symmetrical cleavage of β-carotene into retinal. We identified a polymorphism in the promoter of the BCMO1 gene, inducing differences in BCMO1 mRNA levels (high in adenines (AA) and low in guanines (GG)) and colour in chicken breast muscle. The present study was designed to test whether this polymorphism could affect the response to dietary β-carotene. Dietary β-carotene supplementation did not change the effects of the genotypes on breast muscle properties: BCMO1 mRNA levels were lower and xanthophyll contents higher in GG than in AA chickens. Lower vitamin E levels in the plasma and duodenum, plasma cholesterol levels and body weight were also observed in GG than in AA chickens. In both genotypes, dietary β-carotene increased vitamin A storage in the liver; however, it reduced numerous parameters such as SCARB1 (scavenger receptor class B type I) in the duodenum, BCMO1 in the liver, vitamin E levels in the plasma and tissues, xanthophyll contents in the pectoralis major muscle and carcass adiposity. However, several diet × genotype interactions were observed. In the GG genotype, dietary β-carotene increased ISX (intestine-specific homeobox) and decreased BCMO1 mRNA levels in the duodenum, decreased xanthophyll concentrations in the duodenum, liver and plasma, and decreased colour index and HDL-cholesterol concentration in the plasma. Retinol accumulation following dietary β-carotene supplementation was observed in the duodenum of AA chickens only. Therefore, the negative feedback control on β-carotene conversion through ISX appears as functional in the duodenum of GG but not of AA chickens. This could result in a higher availability of β-carotene in the duodenum of GG chickens, reducing the uptake of xanthophylls, liposoluble vitamins and cholesterol.

Swarming and the expression of phase polyphenism are defining characteristics of locust species. Increases in local population density mediate morphological, physiological and behavioural changes within individuals, which correlate with mass marching of juveniles in migratory bands and flying swarms of adults. The Australian plague locust ( Chortoicetes terminifera ) regularly forms migratory bands and swarms, but is claimed not to express phase polyphenism and has accordingly been used to argue against a central role for phase change in locust swarming. We demonstrate that juvenile C. terminifera express extreme density-dependent behavioural phase polyphenism. Isolated-reared juveniles are sedentary and repelled by conspecifics, whereas crowd-reared individuals are highly active and are attracted to conspecifics. In contrast to other major locust species, however, behavioural phase change does not accumulate across generations, but shifts completely within an individual's lifetime in response to a change in population density.

Diets high in fat and cholesterol are associated with increased obesity and metabolic disease in mice and humans. To study the molecular basis of the metabolic response to dietary fat, 10 inbred strains of mice were fed atherogenic high-fat and control low-fat diets. Liver gene expression and whole animal phenotypes were measured and analyzed in both sexes. The effects of diet, strain, and sex on gene expression were determined irrespective of complex processes, such as feedback mechanisms, that could have mediated the genomic responses. Global gene expression analyses demonstrated that animals of the same strain and sex have similar transcriptional profiles on a low-fat diet, but strains may show considerable variability in response to high-fat diet. Functional profiling indicated that high-fat feeding induced genes in the immune response, indicating liver damage, and repressed cholesterol biosynthesis. The physiological significance of the transcriptional changes was confirmed by a correlation analysis of transcript levels with whole animal phenotypes. The results found here were used to confirm a previously identified quantitative trait locus on chromosome 17 identified in males fed a high-fat diet in two crosses, PERA × DBA/2 and PERA × I/Ln. The gene expression data and phenotype data have been made publicly available as an online tool for exploring the effects of atherogenic diet in inbred mouse strains ( http://cgd-array.jax.org/DietStrainSurvey ).

Maintenance of carbohydrate balance via changes in CO2 output volume was investigated in locusts using a flow-through respirometer. The effect of an imbalance in the dietary protein to digestible carbohydrate ratio on expired CO2 levels was measured in locusts fed one of two synthetic diets [7% protein, 21% digestible carbohydrate (7:21) and 21% protein, 7% digestible carbohydrate (21:7)]. Additionally, the effect of dietary dilution was investigated by feeding locusts one of two diets with a close-to-optimal ratio of protein to carbohydrate, one containing 7% protein and 7% digestible carbohydrate (7:7) and the other containing 21% protein and 21% digestible carbohydrate (21:21). For insects fed unbalanced diets, a higher CO2 output volume was measured during feeding on diet 7:21 when compared with insects fed on diet 21:7. Locusts also expired a greater volume of CO2 during the entire 2h observation period. This response is consistent with specific metabolic control of carbohydrate balance via enhanced respiration. For insects fed balanced diets, the total volume of CO2 expired over the duration of a meal was greater for insects fed diet 7:7 than for those fed diet 21:21, although this was due entirely to meals lasting longer on the more dilute diet. However, the basal level of respiration rate was greater for insects fed diet 21:21 and, as a result, over the entire 2h period, CO2 output volume did not differ between locusts fed diet 7:7 or 21:21. A possible mechanism for enhanced CO2 output volume on the nutritionally unbalanced diet was investigated, namely triglyceride/fatty-acid substrate cycling. There was no evidence for the presence of the thermogenic effect of this particular cycle on locusts as a means for dealing with excess ingested carbohydrate.

The effects of various sources of dietary fibre on the high glycaemic index of an Israeli ethnic food, melawach, were investigated in subjects with non-insulin-dependent diabetes mellitus (NIDDM). Locust-bean (Ceratonia siliqua) gum significantly decreased the glucose response to, and glycaemic index of, melawach in these diabetic subjects (P < 0·05). It also tended to decrease their insulinaemic response and insulinaemic index, but differences were not significant. Dietary fibre from lupin (Lupinus albus) and insoluble maize-cob fibre did not affect glucose and insulin levels in NIDDM volunteers. Subjects with a BMI < 30 kg/m2 exhibited similar glucose, but not insulin, responses to fibre. Locust-bean gum had no significant effect on glycaemic response in NIDDM subjects with a BMI > 30 kg/m2, whereas insulinaemic response decreased. The results indicate that foods containing the same nutrients in almost the same amounts, but differing in added dietary fibre, lead to different physiological responses in diabetic subjects. Furthermore, insulin response should be considered when fibre is incorporated into the diabetic's diet.

Substratum vibrations elicit a fast startle response in unrestrained quiescent desert locusts (Schistocerca gregaria). The response is graded with stimulus intensity and consists of a small, rapid but conspicuous movement of the legs and body, but it does not result in any positional change of the animal. With stimuli just above threshold, it begins with a fast twitch of the hindlegs generated by movements of the coxa-trochanter and femur-tibia joints. With increasing stimulus intensity, a rapid movement of all legs may follow, resulting in an up-down movement of the whole body. The magnitude of both the hindleg movement and electromyographic recordings from hindleg extensor and flexor tibiae muscles increases with stimulus amplitude and reaches a plateau at vibration accelerations above 20 m s(−)(2) (peak-to-peak). Hindleg extensor and flexor tibiae muscles in unrestrained animals are co-activated with a mean latency of 30 ms. Behavioural thresholds are as low as 0. 47 m s(−)(2) (peak-to-peak) at frequencies below 100 Hz but rise steeply above 200 Hz. The response habituates rapidly, and inter-stimulus intervals of 2 min or more are necessary to evoke maximal reactions. Intracellular recordings in fixed (upside-down) locusts also revealed co-activation of both flexor and extensor motor neurones with latencies of approximately 25 ms. This shows that the neuronal network underlying the startle movement is functional in a restrained preparation and can therefore be studied in great detail at the level of identified neurones.

Genetic variation may explain the heterogeneity in the lipid response to dietary change. A systematic literature review found 79 articles on dietary intervention studies, 14 articles on observational studies, and 22 reviews on diet-gene interactions. The evidence suggests that variation within the genes for apolipoprotein (apo) AI, AIV, B and E may influence the lipid response to dietary change. This study assessed the influence of six polymorphisms within the genes for apo B, apo E and lipoprotein lipase (LPL) on the association between habitual diet and lipid levels in 239 healthy men and women (91 men and 148 women) aged 18-54 years, including 110 twin pairs, who were recruited for a population-based study of coronary heart disease (CHD) risk factors. Diet was assessed by a food frequency questionnaire, which was compared with 4-day weighed records in 41 men and 40 women aged 19-58 years. The nutrients of interest had either a correlation coefficient ≥0.5, ≥50/≤10% in the same/opposite third, a KW30.04. Genotypes were determined by the polymerase chain reaction and digestion with the appropriate enzyme. Significant diet-gene interactions were observed at each of the polymorphic sites, suggesting that genetic variation contributes to the framework within which diet, especially n-3 PUFAs, the P:S ratio and NSP can influence lipid levels. In particular, individuals with the apo B XbaI X+ allele, the apo B signal peptide insertion/deletion D allele, the apo &egr;4 allele, the LPL PvuII P- allele and the LPL S447X X allele may be at greater risk of developing CHD due to their poorer lipid profiles and/or poorer response to diet. At present, it is premature to recommend the use of genotyping in the design of therapeutic diets, however investigating diet-gene interactions will increase our knowledge of the mechanisms involved in the role of diet in reducing CHD risk.

We now consider insect populations, circumpolar mammal populations, seaweed density, agricultural yields, and similar topics. Good reasons exist to link such biological phenomena to solar activity. For one thing, if such meteorological parameters as temperature and precipitation vary with solar activity, life forms sensitive to small changes in these parameters may show dramatic responses. We will examine various claims from the 100 to 200 articles that either provide support for or criticize these types of ideas. The topics generally start at the lower levels of the food chain (i.e., insects) and proceed to the upper levels (i.e., predatory mammals), concluding with agricultural and economic studies. Insect populations are sensitive climate indicators. Paleontologists have used fossilized insects (see, for example, Coope, 1977) to show that very rapid changes in climate can occur in only a few years. Certain species of insects can tolerate only narrow ranges of temperature or precipitation. If meteorological variables alter that range, a new species of insect will replace the old. Insects occupy one of the lower rungs of the food chain, so fluctuations in their numbers may cause corresponding fluctuations in such predators as birds or spiders. Therefore, correlating insect populations with solar activity is a worthwhile venture. In his doctoral treatise, “Über die Beziehungen der Sonnenfleckenperiode zu meteorologischen Erscheinungen” published in 1877, F. G. Hahn argues that locusts will probably appear in temperate regions only during unusually hot and dry years. Hahn shows that European locusts appear preferentially between the years of sunspot minimums up to the next sunspot maximum, an average of about 4 years. For the 7 years from the sunspot maximum to the next sunspot minimum, locusts are scarcer. Since sunspot minimums produced relatively warm temperatures for the years 1800–1862, this suggests that the sun influences European locust populations. E. D. Archibald, who in his later years was a very ardent advocate of sun/climate relationships, extended Hahn’s findings. In a letter to Nature in 1878, Archibald showed that locusts appeared in Europe in 1613, 1690, and 1748–1749. According to Wolf, these dates occur 1 to 3 years after a sunspot minimum, which is consistent with Hahn’s findings.

In recent decades, a growing portion of the world’s population has adopted a diet in which increasing calories come from foods high in fat, sugar, and salt that is highly processed by industrial food companies. These ultra-processed products have become the primary determinants of the rising burden of diet-related diseases such as diabetes, heart disease, and stroke, now the world’s leading killers. This chapter shows how food retailers, restaurant and fast food chains, food manufacturers, and agricultural producers have changed in response to changes in capitalism to make the ultra-processed diet the global norm. The agricultural production for these products is also a leading cause of climate change. The chapter further describes an emerging yet uncoordinated popular response that includes farmers and food workers, consumer cooperatives, local governments, and food justice activists that are seeking alternatives strategies for making healthy food affordable to all.

The roles of diet and environment on health have been known since ancient times. Cancer is both a genetic and an epigenetic disease and a complex interplay mechanism of genetic and environmental factors composed of multiple stages in which gene expression, protein and metabolite function operate synchronically. Disruption of epigenetic processes results in life-threatening diseases, in particular, cancer. Epigenetics involves altered gene expression without any change of nucleotide sequences, such as DNA methylation, histone modifications and non-coding RNAs in the regulation of genome. According to current studies, cancer is preventable with appropriate or balanced food and nutrition, in some cases. Nutrient intake is an environmental factor, and dietary components play an importent role in both cancer development and prevention. Due to epigenetic events induce changes in DNA and thus influencing over all gene expression in response to the food components, bioactive compounds and phytochemicals as potent antioxidants and cancer preventive agents have important roles in human diet. Several dietray components can alter cancer cell behavior and cancer risk by influencing key pathways and steps in carcinogenesis, including signaling, apoptosis, differentiation, or inflammation. To date, multiple biologically active food components are strongly suggested to have protective potential against cancer formation, such as methyl-group donors, fatty acids, phytochemicals, flavonoids, isothiocyanates, etc. Diet considered as a source of either carcinogens that are present in certain foods or acting in a protective manner such as vitamins, antioxidants, detoxifying substances, chelating agents etc. Thus, dietary phytochemicals as epigenetic modifiers in cancer and effects of dietary phytochemicals on gene expression and signaling pathways have been widely studied in cancer. In this chapter, current knowledge on interactions between cancer metabolism, epigenetic gene regulation, and how both processes are affected by dietary components are summerized. A comprehensive overview of natural compounds with epigenetic activity on tumorogenesis mechanisms by which natural compounds alter the cancer epigenome is provided. Studies made in epigenetics and cancer research demonstrated that genetic and epigenetic mechanisms are not separate events in cancer; they influence each other during carcinogenesis, highlighting plant-derived anticancer compounds with epigenetic mechanisms of action, and potential use in epigenetic therapy. Recent investigations involving epigenetic modulations suggest that diet rich in phytochemicals not only reduce the risk of developing cancer, but also affect the treatment outcome.

The transition of humankind from mainly rural to urban living has various implications for health and disease among populations. Losing certain environmental exposures from the countryside, while getting new urban exposures provide both risks and opportunities. The rapid pace of urbanization has caused a mismatch in human adaptive capacity, for example resulting in higher prevalence of diabetes in cities in various parts of the world. This can partly be explained by a change in lifestyle related to diet and physical activity associated with urban living. Also mental disorders, like schizophrenia and depression are more common in urban areas. A potential biological explanation may be structural and functional changes in certain brain structures, as a response to urban environments, rendering a higher vulnerability to social stress. Recent neuroscientific studies have indicated that this explanation is plausible.

<em>Abstract.</em>—Prey selection and diet are highly plastic and can vary with temporal and spatial differences in competition or prey availability. This study investigated the possibility that the trophic position of Smallmouth Bass <em> Micropterus dolomieu </em>might change in response to systematic, hierarchical variation in community structure in stream networks. We hypothesized that a shift toward increased insectivory and decreased piscivory would be observed in smaller streams, resulting in a lower trophic position of Smallmouth Bass and reflecting differences in community structure and prey availability. We applied a combination of diet analyses and stable isotope methods to compare prey selection and trophic position of Smallmouth Bass across a range of stream sizes. Stable isotope analyses indicated that Smallmouth Bass trophic position was slightly elevated in smaller watersheds, contradicting our initial hypothesis. However, differences in average trophic position in watershed size categories were small (ranging from 3.6 to 3.8) and of limited ecological significance. Isotopic niche width did not vary among stream size categories, and gut content analyses revealed no differences in frequency of occurrence of fish, crayfish, or insects (larvae and adults). Collectively these results indicate that trophic position, and perhaps trophic niche, of Smallmouth Bass are consistent across hierarchical variation in stream size and habitat.

<em>Abstract.</em>—Fish assemblages in Atlantic coastal rivers have undergone extensive ecological change in the last two and a half centuries due to human influence, including extirpation of many migratory fish species, such as river herring <em> Alosa </em>spp. and introduction of nonnative piscivores, notably Smallmouth Bass <em> Micropterus dolomieu</em>. Recently, dam removals and fish passage improvements in the Penobscot River, Maine, have allowed river herring to return to reaches of the river that have been inaccessible since the late 19th century. Alosine populations have increased and this trend is anticipated to continue. This may increase forage in the system which could potentially increase growth for Smallmouth Bass, the dominant piscivore. We examined the diet and growth of Smallmouth Bass collected from areas of the Penobscot River watershed with and without access to river herring as prey. We collected 765 Smallmouth Bass throughout 2015, examined the stomach contents of 573 individuals, and found notable differences in diet among three river reaches with common seasonal trends. Juvenile river herring composed an average of 19% (SE = ±6%) of stomach contents by mass from Smallmouth Bass collected in the freshwater tidal area but were rarely observed in the diets upstream. We used estimates from von Bertalanffy growth models to examine differences in growth among reaches and found that asymptotic length was the longest (425 mm TL) in the Tidal reach where access to river herring was unrestricted. We then used these data to predict changes to growth associated with increased access to juvenile river herring prey with bioenergetics models. Results indicated that substituting juvenile river herring for less energy-dense prey (e.g., invertebrates) may lead to increases in seasonal growth throughout the watershed as river herring populations continue to rebound in response to dam removal. Our results provide insight into the diet and growth of Smallmouth Bass in a large New England river, and provide a foundation for future work investigating unfolding changes to these characteristics following recent dam removals.

A cohort study is one in which the outcome (usually disease status) is ascertained for groups of individuals defined on the basis of their exposure. At the time exposure status is determined, all must be free of the disease. All eligible participants are then followed up over time. Since exposure status is determined before the occurrence of the outcome, a cohort study can clarify the temporal sequence between exposure and outcome, with minimal information bias. The historical and the population cohort study (Box 9.1) are efficient variants of the classical cohort study described above, which nevertheless retain the essential components of the cohort study design. The exposure can be dichotomous [i.e. exposed (to obstetric complications at birth) vs. not exposed], or graded as degrees of exposure (e.g. no recent life events, one to two life events, three or more life events). The use of grades of exposure strengthens the results of a cohort study by supporting or refuting the hypothesis that the incidence of the disease increases with increasing exposure to the risk factor; a so-called dose–response relationship. The essential features of a cohort study are: ♦ participants are defined by their exposure status rather than by outcome (as in case–control design); ♦ it is a longitudinal design: exposure status must be ascertained before outcome is known. The classical cohort study In a classical cohort study participants are selected for study on the basis of a single exposure of interest. This might be exposure to a relatively rare occupational exposure, such as ionizing radiation (through working in the nuclear power industry). Care must be taken in selecting the unexposed cohort; perhaps those working in similar industries, but without any exposure to radiation. The outcome in this case might be leukaemia. All those in the exposed and unexposed cohorts would need to be free of leukaemia (hence ‘at risk’) on recruitment into the study. The two cohorts would then be followed up for (say) 10 years and rates at which they develop leukaemia compared directly. Classical cohort studies are rare in psychiatric epidemiology. This may be in part because this type of study is especially suited to occupational exposures, which have previously been relatively little studied as causes of mental illness. However, this may change as the high prevalence of mental disorders in the workplace and their negative impact upon productivity are increasingly recognized. The UK Gulf War Study could be taken as one rather unusual example of the genre (Unwin et al. 1999). Health outcomes, including mental health status, were compared between those who were deployed in the Persian Gulf War in 1990–91, those who were later deployed in Bosnia, and an ‘era control group’ who were serving at the time of the Gulf war but were not deployed. There are two main variations on this classical cohort study design: they are popular as they can, depending on circumstances, be more efficient than the classical cohort design. The population cohort study In the classical cohort study, participants are selected on the basis of exposure, and the hypothesis relates to the effect of this single exposure on a health outcome. However, a large cohort or panel of subjects are sometimes recruited and followed up, often over many years, to study multiple exposures and outcomes. No separate comparison group is required as the comparison group is generally an unexposed sub-group of the panel. Examples include the British Doctor's Study in which over 30,000 British doctors were followed up for over 20 years to study the effects of smoking and other exposures on health (Doll et al. 1994), and the Framingham Heart Study, in which residents of a town in Massachusetts, USA have been followed up for 50 years to study risk factors for coronary heart disease (Wolf et al. 1988). The Whitehall and Whitehall II studies in the UK (Fuhrer et al. 1999; Stansfeld et al. 2002) were based again on an occupationally defined cohort, and have led to important findings concerning workplace conditions and both physical and psychiatric morbidity. Birth cohort studies, in which everyone born within a certain chronological interval are recruited, are another example of this type of study. In birth cohorts, participants are commonly followed up at intervals of 5–10 years. Many recent panel studies in the UK and elsewhere have been funded on condition that investigators archive the data for public access, in order that the dataset might be more fully exploited by the wider academic community. Population cohort studies can test multiple hypotheses, and are far more common than any other type of cohort study. The scope of the study can readily be extended to include mental health outcomes. Thus, both the British Doctor's Study (Doll et al. 2000) and the Framingham Heart Study (Seshadri et al. 2002) have gone on to report on aetiological factors for dementia and Alzheimer's Disease as the cohorts passed into the age groups most at risk for these disorders. A variant of the population cohort study is one in which those who are prevalent cases of the outcome of interest at baseline are also followed up effectively as a separate cohort in order (a) to study the natural history of the disorder by estimating its maintenance (or recovery) rate, and (b) studying risk factors for maintenance (non-recovery) over the follow-up period (Prince et al. 1998). Historical cohort studies In the classical cohort study outcome is ascertained prospectively. Thus, new cases are ascertained over a follow-up period, after the exposure status has been determined. However, it is possible to ascertain both outcome and exposure retrospectively. This variant is referred to as a historical cohort study (Fig. 9.1). A good example is the work of David Barker in testing his low birth weight hypothesis (Barker et al. 1990; Hales et al. 1991). Barker hypothesized that risk for midlife vascular and endocrine disorders would be determined to some extent by the ‘programming’ of the hypothalamo-pituitary axis through foetal growth in utero. Thus ‘small for dates’ babies would have higher blood pressure levels in adult life, and greater risk for type II diabetes (through insulin resistance). A prospective cohort study would have recruited participants at birth, when exposure (birth weight) would be recorded. They would then be followed up over four or five decades to examine the effect of birth weight on the development of hypertension and type II diabetes. Barker took the more elegant (and feasible) approach of identifying hospitals in the UK where several decades previously birth records were meticulously recorded. He then traced the babies as adults (where they still lived in the same area) and measured directly their status with respect to outcome. The ‘prospective’ element of such studies is that exposure was recorded well before outcome even though both were ascertained retrospectively with respect to the timing of the study. The historical cohort study has also proved useful in psychiatric epidemiology where it has been used in particular to test the neurodevelopmental hypothesis for schizophrenia (Jones et al. 1994; Isohanni et al. 2001). Jones et al. studied associations between adult-onset schizophrenia and childhood sociodemographic, neurodevelopmental, cognitive, and behavioural factors in the UK 1946 birth cohort; 5362 people born in the week 3–9 March 1946, and followed up intermittently since then. Subsequent onsets of schizophrenia were identified in three ways: (a) routine data: cohort members were linked to the register of the Mental Health Enquiry for England in which mental health service contacts between 1974 and 1986 were recorded; (b) cohort data: hospital and GP contacts (and the reasons for these contacts) were routinely reported at the intermittent resurveys of the cohort; (c) all cohort participants identified as possible cases of schizophrenia were given a detailed clinical interview (Present State examination) at age 36. Milestones of motor development were reached later in cases than in non-cases, particularly walking. Cases also had more speech problems than had noncases. Low educational test scores at ages 8,11, and 15 years were a risk factor. A preference for solitary play at ages 4 and 6 years predicted schizophrenia. A health visitor's rating of the mother as having below average mothering skills and understanding of her child at age 4 years was a predictor of schizophrenia in that child. Jones concluded ‘differences between children destined to develop schizophrenia as adults and the general population were found across a range of developmental domains. As with some other adult illnesses, the origins of schizophrenia may be found in early life’. Jones' findings were largely confirmed in a very similar historical cohort study in Finland (Isohanni et al. 2001); a 31 year follow-up of the 1966 North Finland birth cohort (n = 12,058). Onsets of schizophrenia were ascertained from a national hospital discharge register. The ages at learning to stand, walk and become potty-trained were each related to subsequent incidence of schizophrenia and other psychoses. Earlier milestones reduced, and later milestones increased, the risk in a linear manner. These developmental effects were not seen for non-psychotic outcomes. The findings support hypotheses regarding psychosis as having a developmental dimension with precursors apparent in early life. There are many conveniences to this approach for the contemporary investigator. ♦ The exposure data has already been collected for you. ♦ The follow-up period has already elapsed. ♦ The design maintains the essential feature of the cohort study, namely that information bias with respect to the assessment of the exposure should not be a problem. ♦ As with the Barker hypothesis example, historical cohort studies are particularly useful for investigating associations across the life course, when there is a long latency between hypothesized exposure and outcome. Despite these important advantages, such retrospective studies are often limited by reliance on historical data that was collected routinely for other purposes; often these data will be inaccurate or incomplete. Also information about possible confounders, such as smoking or diet, may be inadequate.

Diet-related disease, climate change, and environmental degradation exact an enormous toll on human and planetary health. These challenges could be addressed in part by shifting what we eat and how we produce food, yet key questions remain about how to make such transitions effective, equitable, and sustainable. To help answer these questions, investments in “sustainable nutrition science”—research and education at the intersection of nutrition, food production, and climate and environment—are urgently needed. However, the Union of Concerned Scientists has found that US public funding for sustainable nutrition science is severely limited, totaling an estimated $16 million annually between 2016 and 2019, and recommends more than tripling that amount in response to our devastating public health and environmental crises.