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PubMed1988

Dietary fat and the beta-adrenergic-mediated chronotropic response in the rat.

We have investigated the effect of dietary fat on isoproterenol-stimulated and propranolol-inhibited heart rate in the rat. In the first experiment, weanling male Sprague-Dawley rats were fed diets containing 10% butter (10B), 10% corn oil (10C) or 9% butter/1% corn oil (10M) for 4 wk. Heart rate was determined in response to increasing i.v. doses of isoproterenol. The percent stimulation at the highest dose of isoproterenol (100 microM) was found to be significantly higher (P less than 0.05) in the 10C-fed group than either the 10B- and 10M-fed groups. A similar study investigated the effect of propranolol inhibition of heart rate in low-fat (10C and 10B) as well as high-fat (25C) corn oil- and high-fat (25B) butter-fed animals. Heart rate was elevated with a constant i.v. infusion of isoproterenol and the inhibitory effect of propranolol was determined. The ED50 was found not to depend on the level of fat, but was found to be significantly lower in the corn oil-fed animals than in those red butter fat (P less than 0.05). Thus, animals appear to be more sensitive to these beta-adrenergic agonists/antagonists when fed a diet containing corn oil rather than butter fat as the lipid source.

Animals↗

PubMed1992

Dietary fat and breast cancer risk: the feasibility of a clinical trial of breast cancer prevention.

Animal experimental evidence and human ecological data suggest that dietary fat intake is related to breast cancer risk. Epidemiological studies within countries have given inconsistent results but are limited by the restricted range of dietary intake found in Western populations and by error in the measurement of fat consumption. Experimental evidence, derived from controlled clinical trials in which the range of fat intake is increased beyond that seen in most Western populations, is capable of overcoming this limitation of observational epidemiology, and would provide the strongest evidence available concerning the relationship of dietary fat intake to breast cancer risk. Further, such trials are the only means likely to answer the question of whether breast cancer risk in high-risk subjects can be modified by changing dietary fat intake. We describe here several aspects of the feasibility of an experimental approach to this problem, including the identification of subjects at increased risk for breast cancer, and the demonstration that such subjects will enter a clinical trial of dietary fat reduction and comply with a low-fat diet. It is shown that subjects can be recruited and retained in such trials, that satisfactory dietary compliance can be achieved over at least 24 mon and that the subjects selected are at demonstrably increased risk of breast cancer. This finding indicates that it is feasible to test the dietary fat-breast cancer hypothesis experimentally by means of a clinical trial.

Adult↗

PubMed2000

Diet quality of young children who received nutrition education promoting lower dietary fat.

OBJECTIVE: : To evaluate the impact of nutrition education promoting lower dietary fat on the overall diet quality in children using a multidimensional index that measures nutrient and food intakes in relation to US dietary recommendations. DESIGN: : Prospective cohort study with two intervention and two control groups. Children with elevated low density lipoprotein (LDL) cholesterol were randomized to one of two intervention groups or an at-risk control group. The intervention children received either the parent-child autotutorial (PCAT) programme, a 10-week home-based self-instruction nutrition education programme, or nutrition counselling from a registered dietitian. Children with non-elevated plasma cholesterol formed the not-at-risk control group. Dietary and blood data were collected at baseline and at 3 months. SETTING: : Paediatric practices in suburbs north of Philadelphia, PA. SUBJECTS: : Two hundred and twenty-seven 4-10-year-old children with elevated LDL cholesterol between the 80th and 98th percentiles, and 76 age- and gender-matched children with non-elevated plasma cholesterol, were studied. RESULTS: : Children who received PCAT or counselling significantly improved their overall diet quality (-0.6 and -0.4 change in diet quality index (DQI) scores) compared with at-risk control children. Children who received either form of nutrition education were more likely to meet the recommendations for three components of the DQI (total fat, saturated fat, sodium) (OR >1.7), but did not improve their intakes of three components of the DQI (vegetables and fruits, complex carbohydrates, calcium) at 3 months. CONCLUSIONS: : Nutrition education promoting lower dietary fat improved children's overall diet quality. However, several dietary behaviours important for long-term health remained unchanged.

Analysis of Variance↗

PubMed1977

Effect of dietary fats on oxidative phosphorylation and fatty acid profile of rat liver mitochondria.

Hydrogenated coconut oil or safflower seed oil were fed at 20% levels to weanling male albino rats for 2 months. The fatty acid patterns of the liver homogenates, mitochondria and the microsomes were determined by gas chromatography as were also the fatty acid patterns of the liver cholesterol esters and the phospholipids. The mitochondrial phospholipids were fractionated by thin layer chromatography and the fatty acid moieties of the individual phospholipids were screened on a gas chromatograph. The oxidative phosphorylation in the liver mitochondria was determined using glutamate, malate and succinate as substrates. The liver fatty acid pattern, especially that of the subcellular particles, seemed to be dependent upon the dietary fat. The fatty acid composition of the mitochondrial phospholipids varied with the dietary fat. Oxidative phosphorylation for glutamate and malate was higher in the group fed safflower oil compared to that in the group fed saturated fat; in the case of succinate, no such difference was noticed. These results suggest that the changes in the phosphorylation capacity are due to the changes in the mitochondrial phospholipids which reflect the composition of the dietary fat.

Animals↗

PubMed1993

Dietary fat affects weight loss and adiposity during energy restriction in rats.

This study examined the effect of dietary fat during food restriction on weight loss, body composition, and adipose tissue lipoprotein lipase activity (ATLPL). Rats previously fed a high-fat diet were divided into four groups. One group served as baseline controls. The other three groups were fed diets of 12%, 28%, or 45% fat, restricted (R) in amounts to equal 75% of their previous ad libitum energy intake. After 10 wk, body weight loss and reduction of adiposity were significantly less in the 45%-R group compared with the 12%-R group (weight P < 0.05; adiposity P < 0.01). Rats fed restricted amounts of the high-fat diet (45%-R group) retained adiposity equivalent to baseline control rats. ATLPL activity was increased in the 45%-R group compared with baseline control rats. Further studies are needed in humans, but these results suggest that body composition will not be normalized with reduction of energy intake unless dietary fat is also reduced.

Adipose Tissue↗

PubMed1998

Composition of dietary fat affects blood pressure and insulin responses to dietary obesity in the dog.

Cardiovascular and metabolic parameters were evaluated in 15 female spayed dogs before and after they became obese on either a saturated fat (LD, lard, n=8) or unsaturated fat (CO, corn oil, n=7) diet. Body weight and body fat increased significantly in both groups, although no differences occurred between diet groups. Dogs receiving the LD diet exhibited a greater increase in mean arterial pressure than those receiving the CO diet (p<0.01; 15.9 +/- 2.1 vs. 9.8 +/- 3.3 mm Hg increase). The CO diet stimulated a greater increase in heart rate than the LD diet (p<0.05; 32.8 +/- 7.8 vs. 14.1 +/- 5.8 bpm increase). Ganglionic blockade with chlorisondamine caused an increase in HR in both lean groups and in the obese CO group, but not the obese LD group, consistent with a decrease in parasympathetic tone to the heart in the dogs overfed saturated fat. Obesity enhanced the heart rate response to beta-adrenergic stimulation by isoproterenol in the LD, but not CO group. The LD diet increased circulating insulin and decreased insulin sensitivity, whereas the CO diet had no effect on either parameter. These findings suggest that the composition of dietary fat can modulate the autonomic and metabolic adaptations induced by dietary obesity.

Adrenergic beta-Agonists↗

PubMed2000

Dietary fats and immune status in athletes: clinical implications.

Athletes are competitive, train at very high levels with inadequate rest, consume too few calories, avoid fats, and may be at increased risk of infections. The immune system is sensitive to both fat intake and intense exercise, suggesting that athletes may have suppressed immune function. It has been reported that many athletes consume about 25% fewer calories than the estimated expenditure, leading to low intakes of some essential micronutrients and fats. Acute exercise has been shown to increase inflammatory and decrease antiinflammatory immune factors and may increase oxidant stress. Chronic exercise appears to improve immune competence. Lipids are powerful mediators of the immune system, and they may modulate the immunosuppressive effects of strenuous exercise. Studies have shown that a low-fat high-carbohydrate diet (15% fat, 65% CHO, 20% protein of total calories), typically eaten by athletes, increases inflammatory and decreases antiinflammatory immune factors, depresses antioxidants, and negatively affects blood lipoprotein ratios. Increasing total caloric intake by 25% to match energy expenditure and the dietary fat intake to 32% in athletes appears to reverse the negative effects on immune function and lipoprotein levels reported on a low-fat diet. Increasing the dietary fat intake of athletes to 42%, while maintaining caloric intake equal to expenditure, does not negatively affect immune competency or blood lipoproteins, whereas it improves endurance exercise performance at 60-80% of VO2max in cyclists, soldiers, and runners. There is no evidence that higher fat intakes (up to 42% of total calories), in calorically balanced diets, increase the risk of cancer, but studies are needed to determine whether the beneficial effects of higher fat diets in athletes reduce their rate of infections.

Antioxidants↗

PubMed1987

In vivo lipogenesis of genetically lean and fat chickens: effects of nutritional state and dietary fat.

In vivo lipogenesis was estimated in liver and carcass of male chickens selected for leanness (LL) or fatness (FL) by use of tritiated water. Effects of nutritional state and of a high fat diet (90 g/kg) were examined. Different classes of liver lipids were also measured. Fed birds exhibited enhanced hepatic lipogenesis, which was more pronounced in FL than in LL birds (+73%, mean of three experiments). Extrahepatic lipogenesis was poorly influenced by nutritional state in LL birds and not modified in FL ones. The high fat diet induced a fall in liver triacylglycerol and reduced de novo lipogenesis more drastically in liver than in carcass of both lines. Reduction of carcass lipogenesis was less pronounced in FL than in LL. Starvation led to a fall in liver triacylglycerols, nonesterified fatty acids and free cholesterol. The fat diet had similar but less pronounced effects. In most circumstances FL chickens exhibited a higher liver triacylglycerol content than LL ones. Comparison of fed and refed birds 100 min after the beginning of refeeding showed that de novo lipogenesis did not reach a plateau and differences between lines were still not significant.

Animal Feed↗

PubMed1998

[Effects of dietary fat saturation on levels of plasma lipoprotein (a) and lipids].

BACKGROUND: Lipoprotein (a) (Lp[a]) is a known risk factor for coronary heart disease. Lp(a) plasma concentration mainly depends on genetic polymorphism. The aim of this study was evaluate the effect of dietary fat saturation on Lp(a) plasma concentration. SUBJECTS AND METHODS: Forty two subjects (eighteen women and twenty four men) were placed in four consecutive 5 weeks diet periods. Energy intake from proteins, carbohydrates and fats was constant during the study and there were only changes on fatty acids composition. First period was enriched in saturated fatty acids (SFA), second period in monounsaturated fatty acids (MUFA) and third and fourth periods were enriched in polyunsaturated fatty acids (PUFA). Fourth period was also enriched in PUFA n-3 (blue fish). RESULTS: Changes on dietary fat saturation had a significant effect on plasma lipids and lipoproteins. Lp(a) plasma concentration was minimum in SFA phase (6.8 [SD 7.3] mg/dl), increasing during MUFA phase (8.7 [8.5] mg/dl) and was maximum in PUFA n-6 and PUFA n-3 (11.5 [11.1] and 12.7 [11.9] mg/dl, respectively) (p < 0.0001). CONCLUSIONS: Changes on dietary fat saturation significantly modify Lp(a) plasma concentration. These variations went in opposite direction to LDL-cholesterol modifications and were clinically irrelevant.

Adult↗

PubMed1994

Dietary fat influences the effect of zinc deficiency on liver lipids and fatty acids in rats force-fed equal quantities of diet.

Previous studies showed that zinc deficiency influences the fatty acid composition of rat tissues, but the influence of dietary fat on the effects of zinc deficiency was not considered at that time. The present study was therefore conducted to investigate the effect of zinc deficiency on lipid concentrations in the liver and on fatty acid composition of liver phospholipids in rats fed diets containing coconut oil or fish oil, using a bifactorial experimental design. To ensure an adequate food intake all rats were force-fed. The zinc-deficient rats fed the coconut oil diet developed fatty livers, whereas zinc-deficient animals fed the fish oil diet did not. The zinc-deficient rats in both dietary fat groups had lower levels of linoleic acid, arachidonic acid and total (n-6) fatty acids in the liver phospholipids, especially in the phosphatidylcholine, but greater concentrations of (n-3) fatty acids compared with zinc-adequate controls. We conjecture that zinc deficiency influences incorporation of polyunsaturated fatty acids into phosphatidylcholine. The lower levels of arachidonic acid are replaced in the zinc-deficient animals fed a coconut oil diet by docosapentaenoic and docosahexaenoic acids and in the zinc-deficient animals fed a fish oil diet by eicosapentaenoic acid. The replacement of arachidonic acid by other fatty acids in the phospholipids is likely to have implications for prostaglandin synthesis. The study shows that the type of dietary fat influences the effects of zinc deficiency on fatty acid composition and especially on lipid concentrations in the liver.

Animals↗

PubMed1999

Dietary fat and prostate cancer: current status.

Efforts to elucidate the causes of prostate cancer have met with little success to date. All that is known with certainty is that the incidence increases exponentially with age, varies by geography and by race or ethnicity, and is higher among men whose father or brother had the disease. Because the incidence changes in migrants and their offspring, exogenous factors certainly contribute to the risk of prostate cancer. Early epidemiologic studies implicated dietary fat as a likely causal factor for this cancer. However, scientific support for such an association has diminished in recent years as more epidemiologic evidence has accrued. Accordingly, we reviewed the relevant English language literature on this topic, including epidemiologic and animal studies, as well as current concepts regarding the involvement of fat in carcinogenesis to re-examine the fat-prostate cancer hypothesis. We conclude that dietary fat may indeed be related to prostate cancer risk, although the specific fat components that are responsible are not yet clear. Given the diverse effects of fatty acids on cellular biology and chemistry, it seems likely that the relationship is complex, involving the interplay of fat with other dietary factors, such as antioxidant vitamins and minerals, or with genetic factors that influence susceptibility. Some suggestions for further research are offered.

Dietary Fats↗

PubMed2001

Inherent capacity for lipogenesis or dietary fat retention is not increased in obesity-prone rats.

Obesity results from positive energy balance and, perhaps, abnormalities in lipid and glycogen metabolism. The purpose of this study was to determine whether differences in lipogenesis, retention of dietary fat, and/or glycogenesis influenced susceptibility to dietary obesity. After 1 wk of free access to a high-fat diet (HFD; 45% fat by energy) rats were separated on the basis of 1 wk body weight gain into obesity-prone (OP; > or =48 g) or obesity-resistant groups (OR; < or =40 g). Rats were either studied at this time (OR1, OP1) or continued on the HFD for an additional 4 wk (OR5, OP5). Weight gain and energy intake were greater (P < or = 0.05) in OP vs. OR at both 1 (53 +/- 2 vs. 34 +/- 1 g; 892 +/- 27 vs. 755 +/- 14 kcal) and 5 (208 +/- 7 vs. 170 +/- 7 g; 4,484 +/- 82 vs. 4,008 +/- 72 kcal) wk, respectively. Rats were injected with (3)H(2)O and were either provided free access to an HFD meal containing labeled fatty acids (fed; n = 10 or 11/group) or were fasted (n = 10/group) overnight. The amount of food or (14)C tracer eaten overnight was equivalent between OP and OR rats. In liver, the fraction of (3)H retained in glycogen or lipid was not significantly different between OR and OP groups. Retention of dietary fat in the liver was not increased in OP rats. In adipose tissue, retention of (3)H was approximately 49% greater (P < or = 0.05) in OP1 vs. OR1 and approximately 30% greater in OP5 vs. OR5, but retention of dietary fat was not elevated in OP vs. OR. At the same time, fat pad weight (sum of epididymal, retroperitoneal, mesenteric) was 49% greater in OP1 rats vs. OR1 rats and 65% greater in OP5 vs. OR5 rats (P < or = 0.05). Thus a greater capacity for lipogenesis or retention of dietary fat does not appear to be included in the OP phenotype. The characteristic increase in energy intake associated with OP rats appears to be necessary and critical to accelerated weight and fat gain.

Adipose Tissue↗

PubMed1987

Dietary fat and breast cancer in the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study.

The relationship between dietary fat intake and breast cancer incidence was examined in the National Health and Nutrition Examination Survey I (NHANES I) Epidemiologic Follow-up Study cohort. This cohort is derived from adults (greater than or equal to 25 yr) examined in the NHANES I (1970-75) cross-sectional survey of the U.S. population and provides a mean follow-up time of 10 years. An analytic sample of 5,485 women, including 99 breast cancer cases (34 premenopausal and 65 postmenopausal at NHANES I baseline), was examined for associations with dietary intake of fat, percent energy from fat, total energy, saturated fat, polyunsaturated fat, monounsaturated fat, and cholesterol on the basis of a 24-hour recall administered at the baseline NHANES I examination. No significant differences in dietary fat intake between cases and noncases were evident when mean intakes for each group were compared. For total fat (g) and saturated fat (g), a significant inverse association was indicated in proportional hazards analyses. Adjustment of fat for total energy intake resulted in a smaller effect that was no longer statistically significant. Adjustment for accepted breast cancer risk factors did not change these findings. This prospective study of a sample from the U.S. population does not support the hypothesis that high dietary fat intake increases breast cancer risk. Indeed, some lower risk associated with high fat intake may be indicated, although this result may be influenced by methodologic problems with the dietary assessment.

Adult↗

PubMed1984

The effect of dietary fat saturation on plasma and hepatic lipoproteins in the rat.

Semipurified diets containing 10% kilocalories from either safflower oil (SO), corn oil (CO), olive oil (OO) or palm oil (PO) were fed to weanling male rats for 2 weeks. The effects of dietary fat saturation on plasma lipids and lipoproteins were: 1) Nonfasted plasma cholesterol concentration was higher in rats fed OO (mean +/- SEM = 81.0 +/- 2.9 mg/dl) vs. CO (67.5 +/- 2.9); 2) plasma chylomicron cholesterol concentration was higher in rats fed OO vs. SO and CO, with PO values in between; and 3) the cholesterol concentration of plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL) did not differ among groups. The effects of dietary fat saturation on hepatic lipoproteins (determined by liver perfusion techniques) were: 1) hepatic higher density lipoprotein (d = 1.006-1.21 g/ml) cholesterol production was greater in rats fed SO and CO vs. PO [19.1 +/- 1.2, 17.2 +/- 0.8 and 13.7 +/- 1.6 micrograms/(g liver X 1.5 hour), respectively]; 2) there was no difference in hepatic VLDL cholesterol production among groups; and 3) the ratio of cholesterol to protein of hepatic VLDL and the higher density lipoprotein fraction was higher in rats fed diets rich in polyunsaturated fatty acids versus saturated fatty acids. Dietary fat saturation had no effect on carcass and liver cholesterol concentrations. Since differences in hepatic lipoprotein production were not reflected in plasma lipoprotein patterns, these results suggest that extrahepatic lipoprotein metabolism differs in rats fed diets containing fatty acids of varying saturation.

Animals↗

PubMed1994

Effects of dietary fat levels on the absorption and tissue accumulation of probucol in the rat.

The effects of dietary fat level on the absorption and tissue accumulation of probucol (PB, CAS 23288-49-5) were studied in male Wistar rats. Addition of 1% PB (w/w) to the diets as compared to the diets without an addition (P) resulted in a decrease in the concentration of both serum and high-density lipoprotein (HDL) cholesterol as well as TBA-reactive substances (TBARS), without influencing food intake or growth. When rats were fed with the PB diet, the apparent intestinal absorption of PB was 7.9%, while the serum PB level was 5 micrograms/ml. The tissue distribution of PB, when expressed per g of tissue, was highest in the adrenal glands, followed by the liver, heart, epididymal adipose tissues, kidneys, lung, spleen, and testes. The addition of 10% olive oil (PBO) to the PB diet (w/w) appeared to double the PB diet-induced increase in apparent intestinal absorption and the serum concentration of PB. Furthermore, compared with the PB diet, the PBO diet caused 3- to 4-fold higher accumulation of PB in the liver and its subcellular fractions and 2-fold higher accumulation in the spleen. However, there was no further accumulation of the drug in the heart, kidneys, lungs, and testes. Incorporation of the drugs into adipose tissues was significantly lower with the PBO diet than with the PB diet. These results suggest that dietary manipulation leads to changes in the intestinal absorption and serum level of PB.

Animals↗

PubMed2001

Comparison of the effect of dietary fat restriction with that of energy restriction on human lipid metabolism.

BACKGROUND: Dietary fat and energy have been implicated as factors controlling circulating total and LDL-cholesterol concentrations. Whether these factors work independently or synergistically in regulating human cholesterol metabolism remains to be fully elucidated. OBJECTIVE: The objective was to determine whether the effects of fat restriction on circulating lipid concentrations and synthesis differ from those of energy restriction in hypercholesterolemic subjects fed controlled diets. DESIGN: Eleven men (LDL > 3.6 mmol/L) participated in a randomized crossover study. Subjects consumed 4 prepared diets, each for 4 wk and separated by 6 wk, that contained either typical amounts of fat and energy (TF), low amounts of fat but adequate energy (LF), low amounts of fat and energy through carbohydrate restriction (LFE), or typical amounts of fat and low energy through carbohydrate restriction (LE). RESULTS: Body weights declined (P < 0.001) after the LE and LFE diets. Total cholesterol concentrations were not significantly different between the diets. LDL cholesterol was lower (P < 0.05) after the LF and LFE diets (8.2% and 8.0%, respectively) than after the TF diet. The LE diet increased HDL cholesterol (46.8%) and decreased triacylglycerols (22.7%), whereas the LF diet increased triacylglycerols (23.6%), relative to the TF diet. LDL:HDL decreased after the LE and LFE diets (P < 0.05). Cholesterol fractional synthesis rates after the LF, LE, and LFE diets were lower (35.2%, 27.7%, and 25.5%, respectively; P < 0.05) relative to the TF diet. CONCLUSION: Reductions in both dietary fat and energy may modify LDL cholesterol by lowering cholesterol biosynthesis; however, the increase in HDL cholesterol and the suppression of triacylglycerol concentrations and LDL:HDL suggests that favorable plasma lipid profiles were also achieved through energy restriction alone.

Adult↗

PubMed1996

Phospholipid fatty acids of brain and liver are modified by alpha-tocopherol and dietary fat in growing chicks.

Dietary fatty acids modify phospholipid fatty acids in brain and liver of growing chickens post-hatching. The effect of vitamin E deficiency on this process is unknown and may be relevant to the pathogenesis of chick nutritional encephalomalacia (NE). Therefore laying hens received a diet low in vitamin E (10 mg alpha-tocopherol/kg feed). Resulting chicks were assigned to nine dietary groups each fed with either oleic (18:1n-9, 58 g/kg), linoleic (18:2n-6, 57 g/kg) or linolenic (18:3n-3, 56 g/kg) acid together with 5. 25 or 125 mg alpha-tocopherol/kg feed. NE affecting the cerebellum only occurred in the group given linoleic acid and 5 mg alpha-tocopherol/kg. In 1-d-old chicks and after 1 and 2 weeks the phospholipid fatty acid composition of liver, cerebrum and cerebellum (additionally after 3 weeks) was determined. The feed fatty acids were incorporated into the liver very efficiently during the first week of life. Unsaturation of liver membranes decreased in the order dietary linolenic > linoleic > oleic acid. In liver, also, the effect of alpha-tocopherol supplementation on phospholipid fatty acids was most pronounced. The unsaturation index increased during deficiency, whereas n-9 fatty acids decreased. In the chicken brain the alterations were delayed and less distinct. The cerebellum phospholipids were rich in n-9 fatty acids and as a whole more saturated in comparison with the cerebrum. Cerebellar unsaturation increased when linolenic or linoleic acid was given. However, NE-producing dietary conditions were not accompanied by specific alterations in cerebellar phospholipid fatty acids due to the alpha-tocopherol content of the diet. Rather the alterations of membrane fatty acids in the liver seem to play a role in the pathogenesis of NE.

Animals↗

PubMed1997

Social worlds, actor-networks and controversy: the case of cholesterol, dietary fat and heart disease.

Knowledge which links dietary fat and cholesterol to coronary heart disease (CHD) has been controversial for more than forty years. While policies advocating fat and cholesterol restriction are now deeply ingrained in affluent western societies, the scientific 'facts' on which they are supposedly based are highly contested. Applying concepts from actor-network theory and the symbolic interactionist social worlds approach, I argue that knowledge and dietary recommendations relating to cholesterol, fat and CHD are the outcome of complex social negotiations which can only be understood in their cultural, commercial and political contexts. Policies were framed in the 1960s before 'proof' of their efficacy was available. Since then, ambiguous experimental results have been shaped to support the policies. I argue that, despite its many attractive features, actor-network theory cannot adequately deal with protracted controversies. Social worlds theory provides a much more useful framework for investigating long debates in which the 'facts' remain elusive.

Anthropology, Cultural↗