Article:
Animals and treatments

 Animal experiments were performed at Imperial College London except for high resolution magic angle spinning (HMRS) experiments which were performed at Instituto de Investigaciones Biomédicas ‘Alberto Sols’ (IIB). Experiments conducted at Imperial College London were approved by Imperial College London, and all animal procedures were performed in accordance with the UK Animals Scientific Procedures Act (1986). IIB experiments were approved by the ethical committee of the Instituto de Investigaciones Biomedicas ‘Alberto Sols’ (and met the guidelines of the national (R.D. 53/2013) and the European Community (2010/62/UE) for care and management of experimental animals. Unless otherwise stated, all experiments were performed in C57BL/6 male mice (6–8 weeks old, Charles River, Margate, UK) that were single-housed under controlled temperature (21–23 oC) and light conditions (12 h light–dark cycle; lights on at 07:00 hours).

 The effect of HF-I versus HF-C on body weight and energy intake

 Mice were randomized and assigned to two different groups (n=12): HFD with cellulose as a control (HF-C), HFD+oligofructose-enriched inulin (Synergy) (HF-I). Synergy is a fructan-based preparation containing both long- and short-chain fructo-oligosaccharides. Synergy was mixed with the HFD individually in the ratio of 1:9. The two diets were isocaloric, each contained the same total energy of 4.6 kcal g−1, with 41.8% energy from fat. The diets were made isocaloric by the addition of cellulose. Nutritional composition of the diet is shown in Table 1. The diets were fed ad libitum for 8 weeks to respective groups of animals. Body weights and food intake were measured three times per week.

 Table 1: Nutritional content of the HFD-C and HFD-I diets. Full table Figures/tables index

 Determination of acetate concentrations in serum and faeces

 SCFAs were determined by gas chromatography in the colonic contents and serum of mice that where freshly culled. The method used was adapted from Richardson et al.35 Briefly, caecal contents were weighed (20–220 μg) and combined with 550 μl of PBS. Samples were vortex mixed for 1 min, centrifuged at 3,000 g for 10 min and the supernatant was collected. To 500 μl supernatant, 25 μl of internal standard and 2-ethylbutyric acid was added to give a final concentration of 5 mmol l−1. Acids were extracted by the addition of 250 μl concentrated hydrochloric acid and 1 ml diethyl ether followed by vortex mixing for 1 min. Samples were centrifuged for 10 min at 3,000 g and the ether layer was removed and transferred to a separate capped vial. N-methyl-N-t-butyldimethylsilyltrifluoroacetamide (MTBSTFA; Sigma) was added (100 μl) before heating at 80 °C for 20 min.

 Gas chromatography was performed on a Hewlett Packard 5890 Series II instrument equipped with a flame ionization detector, split/splitless injector and a 10-m, 0.18 mm ID and 0.20 μm df Rtx-1 (Crossbond 100% dimethyl polysiloxane, Thames Restek UK, Ltd) capillary column. Injector and detector temperatures were 275 oC with the column temperature programmed from 63 °C for 3 min to 190 oC at 10 °C per min. Helium served as the carrier gas (head pressure 135 kPa) and injections (1 μl) were made in the split mode (50:1 split). Peak areas were recorded and all subsequent data manipulation was completed using ChemStation Software (Agilent Technologies, USA). External standards for acetate, propionate, n-butyrate, iso-butyrate, n-valerate and caproate were prepared at concentrations of 25, 12.5, 6.25, 1.25 and 0.625 mM and ethyl butyric acid was used as the internal standard at a concentration of 100 mM. Reported values were normalized according to the weight of original sample used.

 Serum SCFA measurement

 A 100–500-μl aliquot of serum was filtered through a 30-kDa micropartition system (Vivaspin RC VS02H22 filters, Sartorius Inc., Mississauga, ON, Canada) by centrifugation at 14,000 g at 4 °C for 90 min. An internal standard solution (25 μl) consisting of 100 mM ethylbutyrate and 100 mM formic acid was added to 225 μl of the protein-free filtrate supernatant in a 2-ml Hichrom vial (Agilent Technologies, South Queensferry, UK). To measure SCFA, 1 μl of each sample was injected into a 5,890 Series II GC system (HP, Crawley, UK) fitted with a NukolTM Capilllary Column (30 m × 0.53 mm × 1.0 μm, SUPELCOTM Analytical, UK) and flame ionization detector. The carrier gas, helium, was delivered at a flow rate of 14 ml min−1. The head pressure was set at 10 p.s.i. with split injection. Run conditions were: initial temperature 60 °C, 1 min; +20 °C min−1 to 145 °C; +4 °C min−1 to 200 °C, hold 25 min. Peaks were integrated using Agilent ChemStation software (Agilent Technologies, Oxford, UK) and SCFA content quantified by single-point internal standard method. Peak identity and internal response factors were determined using a 1-mM calibration cocktail including acetate, propionate and butyrate.

 PET-CT analysis of acetate biodistribution

 Mice were fasted overnight. Animals received 11C-acetate (~20 MBq) at the beginning of PET scan either through i.v. tail vein (n=3) or colonically by using tubing placed 1 cm into the rectum (n=4). At the time of the scan, animals were anaesthetized with a 2–2% isofluorane–oxygen mix. After the animals were placed in the micro PET/CT scanner (PET/CT (Siemens), a CT scan without contrast was performed, followed by the PET scan and lastly followed by a CT scan where contrast Ultravist 370 (Bayer, AG, Germany) was infused.

 During the scan, animals were maintained at 1–1% isofluorane–oxygen mix and body temperature of 37 °C. The CT had an X-ray source of 80 kVp and 500 μA with exposure time 200 ms and isotropic resolution of 103 μm. The scan consisted of three bed positions with a 20% overlap. The CT scan was used for anatomical data and attenuation correction purposes. The PET system consisted of 64 lutetium oxyothosilicate based detectors blocks arranged in four contiguous rings, with a crystal ring diameter of 16.1 cm and an axial extent of 12.7 cm. Each detector block was composed of a 20 × 20 array of lutetium oxyothosilicate crystals coupled to a position sensitive photomultiplier tube via a light guide. Each crystal was 10 mm long and had a cross-sectional area of 1.51 × 1.51 mm. The crystal pitch was 1.59 mm in both axial and transverse directions. Inveon Research Workplace version 3 (Siemens) was used for data analysis. Images with matrix size 12 × 128, pixel size 0.776 mm2 and slice thickness 0.796 mm were reconstructed from the two-dimensional sinogram by two-dimensional-filtered backprojection using a ramp filter with a nyquist frequency of 0.5. Dynamic framing was used in reconstruction with 20 × 3 s frames, 8 × 30 s frames, 5 × 60 s frames and 10 × 300 s frames. Attenuation correction was also used to correct the image. Reconstructed PET images were then registered onto the CT images. PET signals on the desired region of interest were obtained over the scan period (1 h). Percentage injected dose (% ID per g) was calculated by using the following Equations (1) and (2), where; λ=0.693/T 1/2 , T 1/2 is the half-life of the radionuclide, I t is activity at a given time where I 0 is the starting activity and t is the time passed, C PET is the contrast of the image and ID is the activity of the injected acetate.

 Effect of i.p. acetate on energy intake

 Mice were fasted overnight before receiving either 500 mg kg−1 sodium acetate dissolved in 0.9% saline (n=22) or vehicle control (0.9% saline; n=21) pH 7.0, This dosage of acetate was similar to that used to suppress lipolysis in previous studies and was shown to be well tolerated14. Food intake was measured 1, 2, and 4 h post injection.

 Effect of i.c.v. acetate on energy intake

 Male Wistar rats 190–240 g (specific pathogen free; Charles River) were placed in a stereotaxic frame (David Kopf Instruments) under 0.5-2.5% isoflurane anaesthesia. A hole was drilled using a stereotactically mounted electric drill using coordinates calculated from the Rat Brain Atlas as described previously36, according to the coordinates of Paxinos and Watson37 (0.8 mm posterior to the Bregma in the midline and 6.5 mm below the surface of the skull). A permanent 22-gauge stainless steel cannula (Plastics One Inc., Roanoke, Virginia, USA) projecting to the third cerebral ventricle was implanted. Dental cement was used to hold the cannula in position anchored by three stainless steel screws inserted into the skull. The skin was approximated using nylon sutures. After a 7 day recovery period, animals were handled daily and acclimatized to the injection procedure. To ensure that cannulae were correctly positioned, rats received i.c.v. 150 ng angiotensin II in a 5-μl volume via a 28-gauge stainless steel injector placed into and projecting 1 mm below the tip of the cannula. Rats were observed for a prompt drinking response. A total volume of 5 μl was injected over 1 min to conscious, freely moving rats. For feeding studies, rats (n=15) were fasted overnight and then injected between 09:00 and 10:00 hours with sodium acetate (2.5 μmol) or an equivalent osmotic sodium chloride control (5 μl) and returned to their home cage. Food intake was measured at 1, 2 and 4 h post injection. After a 72-h washout period, rats received either the acetate or sodium chloride in a cross-over manner and food intake measured as previously described.

 Effect of liposome encapsulate acetate on food intake

 Nanoparticle design was based upon our previous studies where PEGylated liposomes were formulated for labelling and visualization of cells38, or specifically designed for preferential uptake in xenograft tumours15. Liposomes were prepared by the thin-film hydration method39. Liposomes were prepared with either acetate (1 M, pH 2.3) to form liposome-encapsulated acetate (LITA) nanoparticles or HEPES for use as a control. Particle size was determined using a Malvern Zetasizer (Malvern Instruments, UK). Quantification of acetate encapsulated within LITA nanoparticles was determined using 1H nuclear magnetic resonance (NMR) spectroscopy. LITA formulation (200 μl) was scanned with addition of albumin that binds to acetate in free solution reducing the NMR signal for the compound40. A liposome-free control solution containing an equivalent concentration of acetate (4 mM) was also scanned with and without the addition of albumin (2 g). LITA solution was scanned following the addition of lactate (5.2 mg sodium lactate) to act as a quantitative control. Spectra were obtained using a Bruker DRX 11.74T NMR spectrometer. Spectra were analysed using MestRe-C NMR spectroscopy software (Santiago de Compostela, Spain).

 To assess short-term biodistribution, a liposome formulation containing an additional 0.1% of a rhodamine–lipid complex (DOPE-Rhodamine: 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-(lissamine rhodamine B sulfonyl) was used to determine biodistibution through ex vivo histological analysis. Samples were collected 4 h post i.p. injection (n=4). No significant accumulation of liposome was observed in the brain of the treated mice despite being present in the liver and heart.

 The effect of acetate on behaviour

 Mice were fasted overnight before receiving either a single i.p. injection of saline, 500 mg kg−1 acetate or 2.5 M LiCl as a positive control for aversive behaviour41 (n=8 per group). The behavioural patterns of each mouse were observed for 15 s every 5 min from the time of injection until 1 h post injection. Behaviours was classified using a modified version of a previously published protocol42. Briefly, behaviours was classified into 10 different categories: feeding, drinking, locomotion (including rearing and climbing), bed making, burrowing, grooming, still, sleeping, head down (animal in abnormal body posture: back hunched, eyes shut or half-shut and pilo erect—indicative of impaired health status) and tremors.

 Acetate tolerance test

 Glucose levels were determined from blood taken from mouse tails using a Glucometer Elite glucometer (Bayer Corp.). Experiments were performed on ad libitum fed mice at 14:00 h as previously described for insulin tolerance tests18 but instead of insulin, animals were injected i.p. with either 500 mg kg−1 sodium acetate or saline control (n=9–10). Blood glucose values were then determined at the times indicated. Results were expressed as fold change of initial blood glucose concentration before injections.

 Plasma PYY and GLP-1 hormone analysis

 All samples were assayed in duplicate and in a single assay to eliminate inter assay variation. Plasma PYY and GLP-1 were assessed using an established in-house radioimmunoassay as described previously43, 44.

 Hypothalamic quantitative PCR

 This was carried out using the methods described by Bewick et al.45 Quantitative reverse transcriptase PCR (RT-qPCR) was used to study the expression of the different target genes. Total RNA was extracted from the whole hypothalami using TRIZOL (Invitrogen) according to the manufacturer’s protocol. All samples were treated by DNaseI (Invitrogen) before the reverse transcription. First-strand cDNAs were prepared using 1 μg RNA and SuperScriptII Reverse Transcriptase (Invitrogen) in the presence of random hexamer and oligo(dT) primers (Promega, Charbonnières-les-Bains, France). The qPCRs were performed using the Light Cycler Fast Start DNA Master SyBR Green I kit (Roche, Meylan, France) in the presence of specific primer pairs that were selected to amplify small fragments (100–200 bp). PCR products were checked for specificity by measuring their melting temperature. Samples (in duplicate) were quantified by comparison with a standard curve obtained by dilutions of purified-specific cDNAs.

 Measurements of AGRP and POMC mRNA expression

 RNA was extracted from dissected hypothalamus using Absolutely RNA microprep kit from Stratagene (La Jolla, CA, USA). The gene transcription for AgRP and POMC in the ARC of the hypothalamus was determined using real-time RT-PCR, and results were expressed as a ratio to the expression of the constitutive gene cyclophilin. The sequences of TaqMan probes and primers for cyclophilin (GenBank accession no. M15933) were: forward primer 5′-CCCACCGTGTTCTTCGACAT; reverse primer 5′-TGCAAACAGCTCGAAGCAGA-3′; and probe 5′-CAAGGGCTCGCCATCAGCCG-3′. For AGRP, they were: forward primer 5′-TTGGCAGAGGTGCTAGATCCA-3′; reverse primer 5′-AGGACTCGTGCAGCCTTACAC-3′; and probe 5′-CGAGTCTCGTTCTCCGCGTCGC-3′. The probe and primers for POMC (assay identification no. Rn00595020_ml) were purchased from Applied Biosystems.

 Manganese-enhanced MRI

 MEMRI was performed using a 9.4-Tesla Varian INOVA imaging system (Varian Inc., USA) as described previously46. A fast spin-echo multi-slice sequence was applied with the following parameters: TR= 600 ms, TE=10 ms, matrix size= 256 × 192, FOV=25 × 25 mm and average=1 acquiring 46 × 0.4 mm thick slices. An array of 66 acquisitions was set up so that the 46 slices were acquired 66 times throughout the infusion. Normalized percentage enhancement in signal intensity was calculated for the ARC, VMH, PVN, periventricular nucleus (PE) and the nucleus of tractus solitarius27, 43.

 Hypothalamic measurement of AMP kinase

 Animals were killed by decapitation, brains were immediately dissected and the hypothalamus was removed and snap-frozen in liquid nitrogen. Frozen tissues (~100 mg) were homogenized in 0.4 ml of ice-cold 50 mm HEPES, pH 7.4, 50 mm sodium fluoride, 5 mm sodium pyrophosphate, 250 mm sucrose, 1 mm EDTA, 1 mm dithiothreitol, 1 mm benzamidine, 1 mm trypsin inhibitor, 0.1% (w/v) phenylmethylsulfonyl fluoride using an UltraTurax homogenizer (3 × 30-s bursts). Insoluble material was removed by centrifugation and the resulting supernatant was used for immunoprecipitation of AMPK and western blot analysis.

 Immunoblotting and antibodies

 Samples were boiled in electrophoresis sample buffer and resolved on polyacrylamide gels. Proteins were transferred into PVDF membrane (Immobilon-FL, Millipore) and blocked with PBS containing 5% skimmed milk powder for 1 h. Antibodies were diluted in 5 ml high salt Tween buffer (20 mM Tris, pH 7.4, 500 mM NaCl and 0.5% Tween (v/v)), and incubated with the membrane. Primary antibodies used for immunoblotting are as follows: anti-AMPK-β1/2 (in-house) (dilutions 1:3,000–1:10,000 for blotting), anti-phospho-ACC (S79) (Cell Signalling, cat. no. 3661), anti-phospho-AMPK (PT172) (Cell Signalling, cat. no. 2535) anti-β-actin (Sigma, cat. no. A5316).

 Primary antibodies were detected using fluorescently linked secondary antibodies (Alexa Fluor, Invitrogen, goat anti rabbit: A21109 and goat anti mouse: A21058). These were visualized using an Odyssey infrared imager (Li-Cor Biosciences). Quantification of results was performed using Odyssey software and expressed as a ratio of the signal obtained with the phospho-specific antibody relative to the appropriate total antibody. Full-length images of cut immunoblots are shown in Supplementary Fig. 1.

 The effect of acetate on hypothalamic metabolism

 [2-13C] acetate (500 mg kg−1) or [U-13C] inulin (100 mg) were administrated to 8–10-week-old C57BL/6J male mice (Charles River, Spain) after an overnight fasting (16 h) either with i.p. (n=18) or by gavage (n=4), respectively. All mice were anaesthetized with 4% isoflurane (3 l per min, 99% oxygen), and cerebral metabolism was arrested within 1.5 s using a high-power (5 kW) microwave fixation system (TMW-6402C, Muromachi Kikai Co. Ltd, Tokyo, Japan) immediately (0 min), 15 and 30 min after acetate, or 180 min after inulin, administrations. Fixed brains were dissected and hypothalamus and remaining brain biopsies were obtained and maintained frozen (−80 °C) until HR-MAS analyses. 13C (125,03 MHz) and 1H HR-MAS (500,13 MHz) spectra were acquired at 11.7 T (4 °C, 4,000 Hz rotation) with a Bruker AVANCE wide bore spectrometer equipped with a MAS accessory (Bruker Biospin, Rheinstetten, Germany). 1H-decoupled 13C HR-MAS spectra were acquired using a pulse-acquire sequence, with WALTZ-16 1H decoupling applied during the acquisition and relaxation delay periods. Conditions were π/4 pulses, 8,192 or 16,384 scans (for [2-13C] acetate or [U-13C] inulin measurements, respectively), 64 k data points, 5 s recycle delay. The 13C spectra were processed with Mestrelab ( http://mestrelab.com/). Chemical shifts of the 13C resonances were referred to the acetate C2 resonance (24.5 p.p.m.), and the 13C incorporation was normalized to the myo-inositol C1+C3 resonance (73.2 p.p.m.), which provides a useful internal reference from which all 13C resonances can be normalized independently of the amount of tissue20, 47, introducing appropriate corrections for nuclear Overhausser enhancement and saturation.

 1H HR-MAS spectra from the same biopsies used for 13C HR-MAS acquisitions were acquired using the Carr-Purcell-Meiboom-Gil sequence. Acquisition parameters were 5 s water pre-saturation, echo time=144 ms, t=1 ms, n=100, 10 kHz spectral width, 32 k data points and 256 scans. Metabolite concentrations were evaluated using a modified version of the LCModel processing software (Linear Combination of Model Spectra, http://s-provencher.com/pages/schtm)48.

 Statistical tests were performed using two-tailed unpaired Student’s t-test between values in the different time points or areas. Observations that fell below the Q1-1.5 × IQR (interquartile range) or above the Q3+1.5 × IQR range (with Q 1 and Q 3 representing the upper and lower quartiles values and IQR, the difference between Q 3 and Q 1 ) were considered outliers and were not taken into account for statistical evaluations.

 Data analysis

 Analyses were performed using Graph Pad Prism (GraphPad Software, San Diego, CA, USA) or Stata (StataCorp LP, College Station, TX, USA). All data was tested for normality using Shapiro–Wilk test. Non-normally distributed data was log transformed to normalize the distribution. Comparison between groups was carried out by two-sided unpaired Student’s t-test for two groups and one-way analysis of variance (ANOVA) with post hoc Tukey or Bonferroni correction if there were more than two groups. I.c.v. cross-over acetate injection studies were compared using a two-sided paired Student’s t-test. Given the cumulative nature of both MEMRI and PET signal intensity data, differences in signal intensity profile between the regions of interest in all experimental groups were analysed using GEE and the Mann–Whitney U-test with commercial statistical software (Stata, version 9.1; StataCorp), which compare profiles for the entirety scan. All results and graphs are expressed as means±s.e.m. Results were considered statistically significant when P<0.05, with the significance level indicated as *P<0.05, **P<0.01 and ***P<0.001 ||||| Peter Cade/Getty

 A study of mouse metabolism suggests that a product of fibre fermentation may be directly affecting the hypothalamus, a region of the brain involved in regulating appetite.

 People have long been told that a diet high in fibre can help to fight obesity, but how it does so has been unclear. “There has been lots of epidemiological information showing a relationship between fibre and obesity, but no one has been able to connect the epidemiological results with actual mechanisms,” says Jimmy Bell, a biochemist at Imperial College London who worked on the research, published today in Nature Communications1.

 Until now, a high-fibre diet was thought to help keep weight down by stimulating the release of appetite-suppressing hormones in the gut2, says Bell, but humans do not seem to show the same increase in these hormones that mice do.

 So Bell and his colleagues decided to look elsewhere. An obvious candidate, they thought, might be one of the products of fibre fermentation in the gut. In particular they focused on the short-chain fatty acid acetate, because it is the most abundant and is known to circulate throughout the bloodstream.

 They fed mice fibre labelled with carbon-13, which has an additional neutron from the more common carbon-12 that gives its nuclei a magnetic spin and therefore makes it easy to track as it progresses through the body's chemical reactions. The fibre was fermented as usual into acetate, which turned up not only in the gut, but also in the hypothalamus, a part of the brain known to be involved in regulating appetite. There, the researchers found, it was metabolized through the glutamine-glutamate cycle, which is involved in controlling the release of neurotransmitters associated with appetite control. The same model has been proposed for acetate metabolism after drinking alcohol.

 The mice fed with large doses of fermentable fibre ate less food, and ended up weighing less than control mice that were fed unfermentable fibre.

 'Simplistic' approach

 William Colmers, an electrophysiologist who studies the effect of neurotransmitters in the hypothalamus at the University of Alberta in Edmonton, Canada, says he thinks that the experimental work is solid, but worries that the results have been over-interpreted. “Much of it is extremely speculative,” he says. For one thing, the dietary fibre levels were around 11%. At that level, “the room would be full of mouse farts”, he says, so the animals may simply have been eating less because they were uncomfortable.

 Colmers adds that the hypothesis of how acetate in the hypothalamus was affecting the release of neurotransmitters to decrease appetite is “a simplistic view of how the nervous system works”. The release of neurotransmitters is “excruciatingly well regulated”, he says, and not as sensitive to manipulation by changes in biochemistry as the authors suggest.

 Although the work was done in mice, Bell says that he sees “no reason” why the same mechanism shouldn’t be at work in humans. “Acetate is known to be metabolized in the human brain, and we have the right microbiota in our gut for the fermentation of fibre,” he says.

 Bell and his colleagues are preparing to test their ideas in people. The question, however, is how much fibre do you have to eat? Most people's diet contains between 10 and 20 grams of fibre a day, and it can be difficult to increase this amount substantially. So Bell and his colleagues are working with companies that are looking into enriching fibre with acetate to boost the digestive system, and into ways of encasing acetate in nanoparticles so that it releases slowly throughout the day to help control appetite. “It’s sort of a way of having your cake, and not eating it,” says Bell. ||||| A pill that switches off hunger is on the horizon after scientists discovered an ‘anti-appetite’ molecule which tells the body to stop eating.

 Researchers at Imperial College discovered that people feel full when eating fruit and vegetables because fibre releases acetate into the gut.

 They believe that a pill derived from acetate could be created to help people cut down on food without experiencing any cravings.

 One in four adults in England is obese and that figure is set to climb to 60 per cent of men and 50 per cent of women by 2050.

 Obesity and diabetes already costs the UK over £5billion every year which is likely to rise to £50 billion in the next 36 years.

 Large amounts of acetate are released when plants and vegetables are digested by bacteria in the colon. The scientists tracked the molecule and found that it eventually ended up in the hypothalamus region of the brain, which controls hunger.

 The new study suggests obesity has become an epidemic because we have replaced the healthy diet of the past with processed food, which does not react with gut bacteria to produce acetate. So the brain does not receive a signal telling it to stop eating.

 The average diet in Europe today contains about 15 g of fibre per day. In Stone Age times it was around 100g per day.

 "Unfortunately our digestive system has not yet evolved to deal with this modern diet and this mismatch contributes to the current obesity epidemic,” said Professor Gary Frost, of Imperial College.

 Although scientists say their research should encourage more people to eat more fruit and vegetables, they also believe it could pave the way for new drugs to help dieters.

 Prof Frost added: "Our research has shown the release of acetate is central to how fibre suppresses our appetite and this could help scientists tackle overeating.

 "The major challenge is to develop an approach that will deliver the amount of acetate needed to suppress appetite but in a form that is acceptable and safe for humans.

 "Developing these approaches will be difficult but it is a good challenge to have and we are looking forward to researching possible ways of using acetate to address health issues around weight gain.”

 The study analysed the effects of a form of dietary fibre called inulin which comes from chicory and sugar beets and is also added to cereal bars.

 Experiments on mice found those fed on a high fat diet with added inulin ate less and gained less weight than animals given a lot of fat diet with no inulin.

 They also noticed that the acetate acculmulates in the hypothalamus of the brain where it triggers a series of chemical events which fire neurons and suppress hunger.

 The research also showed when acetate was injected into the bloodstream, the colon or the brain it reduced the amount of food eaten by the mice.

 Prof Jimmy Bell, of the Medical Research Council, Cambridge, who collaborated in the research, said: "It is exciting we have started to really understand what lies behind fibre's natural ability to suppress our appetite and identified acetate as essential to the process.

 "In the context of the growing rates of obesity in western countries, the findings of the research could inform potential methods to prevent weight gain."

 Acetate is only active for a short amount of time in the body so an ‘acetate pill’ would need to be able to mimic the chemical’s slow release into the gut.

 Prof David Lomas, chair of the MRC's population and systems medicine board, said it is becoming increasingly clear the interaction between the gut and the brain plays a key role in controlling how much food we eat.

 He added: "Being able to influence this relationship, for example using acetate to suppress appetite, may in future lead to new, non surgical treatments for obesity." ||||| TIME Health For more, visit TIME Health

 Scientists have figured out the reason fiber is such a wonder food: It contains an anti-appetite molecule called acetate.

 Acetate, the researchers discovered, is naturally released when fiber is digested in the gut, and when it’s released, it is taken to the brain where it signals us to stop eating.

 Fiber has long been known to satiate appetite and keep us full for longer, but previous research supposed the reason was that it takes longer to digest, keeping us satisfied for longer after we’ve stopped eating. But this new research published in the journal Nature Communications shows that the acetate released when we digest roughage lowers our appetites when it gets directly into our bloodstream, colon or brain.

 The researchers looked at a dietary fiber called inulin, which comes from chicory and sugar beets, and is often present in cereal bars. They fed mice a diet high in fat with additional inulin. These mice ate less and gained less weight than mice who did not consume inulin, and when the scientists took a deeper look, they discovered that the inulin-eating mice had higher levels of acetate in their gut. So, they used PET scans to track the inulin through the mice.

 They discovered that the acetate traveled from the colon to the liver and heart, and finally made it to the the area of the brain that deals with hunger, the hypothalamus region. Using more imaging, they determined that the acetate accumulates and spurs chemical reactions in the brain that send signals that suppress hunger.

 Eating more fiber, found in foods like nuts, oatmeal, beans, lentils, apples and blueberries, is one of the better ways to feel full and satisfied, and can help with weight management. Science says so. |||||Summary:

– Experts have long suggested that fiber keeps us feeling full because it takes a long time to digest, but new research challenges that notion—and may point the way to a new anti-hunger pill. The key is a short-chain fatty acid called acetate, which emerges as fiber is digested. Acetate then makes its way to the brain's hypothalamus, where it builds up and triggers chemical reactions that tell us we're full, Time reports. Researchers reached this conclusion by scanning the progress of a dietary fiber called inulin through the bodies of mice. Those mice who ate fatty diets rich in inulin gained less weight than mice who didn't eat inulin. But one electrophysiologist not related to the study points out that the mice were fed dietary fiber levels of about 11%. He tells Nature that at such a level, "the room would be full of mouse farts"—and perhaps the mice were eating less because they felt gassy. The researchers plan to next test the idea in humans. So could we eventually see an acetate-based diet pill? It's possible, the Telegraph suggests: "The major challenge is to develop an approach that will deliver the amount of acetate needed to suppress appetite but in a form that is acceptable and safe for humans," a researcher says.


Article:

COLUMBUS, Ohio -- Gov. John Kasich on Wednesday announced he has postponed Ronald Phillips' execution date until next summer in order to investigate whether the convicted killer's organs can be donated to family members.

 The governor's decision came one day before the 40-year-old Summit County man was scheduled to be put to death under a newly approved lethal-injection drug cocktail.

 Phillips, sentenced to death in 1993 for raping and killing the 3-year-old daughter of his girlfriend, sought the delay in order to see whether he would be a viable organ donor to his mother, who has kidney disease, and his sister, who has a heart condition, according to the Associated Press.

 Phillips is also willing to donate organs to other people if he couldn't help his relatives, his attorney, Lisa Lagos, told the AP. Lagos said the request wasn't a delaying tactic but an attempt by Phillips to make a final gesture for good.

 The Department of Rehabilitation and Correction had denied Phillips' request earlier this week, citing logistics and security concerns, according to the AP.

 The DRC isn't aware of any other time that an Ohio death-row inmate has made an organ donation, according to spokeswoman JoEllen Smith. However, Smith noted that it has happened in other states such as California.

 In a statement, Kasich said he realized the situation "is a bit of uncharted territory" for Ohio.

 "But if another life can be saved by his willingness to donate his organs and tissues, then we should allow for that to happen," he said.

 Under DRC policy, state prison officials will conduct the initial compatibility tests.

 If a transplant of any non-vital organs is feasible, Phillips would undergo an operation at Ohio State University Medical Center before returning to death row, the governor's office said in a release. His execution has been rescheduled for July 2, 2014 at Southern Ohio Correctional Facility in Lucasville.

 Phillips' execution has drawn increased attention because he was scheduled to be the first person put to death in Ohio using a new and untried lethal-injection cocktail consisting of midazolam, a sedative, and hydromorphone, a morphine derivative.

 The new method was announced last month because of a shortage of pentobarbital caused by European manufacturers' reluctance to sell the drug for executions.

 With Phillips' execution postponed, Dennis McGuire may become the first inmate put to death using the new cocktail. McGuire, a Preble County man convicted of raping, choking and stabbing a pregnant woman in 1989, is scheduled to die Jan. 16, 2014.

 Under the DRC's new protocol, the Southern Ohio Correctional Facility warden must notify department Director Gary Mohr within 14 days of McGuire's execution date whether he has enough pentobarbital to carry out the execution or if the new cocktail must be employed instead. ||||| Convicted child-killer Ronald Phillips was in the Death House and had ordered his last meal when he got the word yesterday: Gov. John Kasich had postponed his execution set for today to determine whether his “nonvital” organs could be harvested as he requested.

 His execution now is scheduled for July 2.

 “His first words were, ‘God is good.’ He feels immense gratitude to the governor,” said Tim Sweeney, the condemned man’s Cleveland attorney.

 Kasich’s action is unprecedented in the nation in the case of an imminent execution, a death-penalty expert said.

 The Republican governor said he halted Phillips’ execution “so that medical experts can assess whether Phillips’ nonvital organs or tissues can be donated to his mother or possibly others.”

 “Ronald Phillips committed a heinous crime for which he will face the death penalty,” Kasich said in a statement less than 18 hours before the condemned man was to be lethally injected using two drugs never before used in combination. “I realize this is a bit of uncharted territory for Ohio, but if another life can be saved by his willingness to donate his organs and tissues, then we should allow for that to happen.”

 The governor said if Phillips “is found to be a viable donor to his mother or possibly others awaiting transplants of nonvital organs, such as kidneys, the procedures would be performed and then he would be returned to Death Row to await his new execution date.”

 There was no immediate comment from Akron Prosecutor Sherry Bevan Walsh, who handled the case.

 Phillips, 40, was to be executed at 10 a.m. today at the Southern Ohio Correctional Facility near Lucasville for the 1993 beating, rape and murder of 3-year-old Sheila Marie Evans, the daughter of his girlfriend at the time. He had exhausted all legal appeals and was moved yesterday to the Lucasville prison, where executions take place. Last night, he was returned to Death Row at the Chillicothe Correctional Institution.

 Sweeney said his client was motivated “by love for his mom and for the desire to do something good. He’s been very remorseful for what he did, thoughtful and reflective over the past couple weeks.”

 He wants to donate a kidney to his mother, who is on dialysis treatment for kidney disease, but is willing to donate to others if that is not possible.

 Sweeney said he wasn’t sure what Phillips can donate, but he said it might include his kidneys, lungs, liver or bone marrow.

 Prisons policy requires that the cost of transplant surgery be paid by Phillips or the organ recipients, not by Ohio taxpayers, spokeswoman JoEllen Smith said. The policy also requires that Phillips’ surgery be performed at the Wexner Medical Center at Ohio State University.

 It is the first time in the United States that an execution was stopped to permit an inmate’s organs to be harvested, said Richard Dieter of the Death Penalty Information Center in Washington, D.C. He said a Delaware inmate, Steven Shelton, was allowed to donate his kidney in 2005, but he was not facing immediate execution.

 Phillips had ordered, but did not have time to eat, his “last meal,” which included pizza with mushrooms, onions and double cheese, spaghetti, corn chips, Dr Pepper, rocky road ice cream and Oreo cheese cake.

 ajohnson@dispatch.com

 @ohioaj |||||
What is a summary?

– A convicted child killer just got a last-minute reprieve from Ohio's governor, thanks to the inmate's unusual request to be an organ donor. Ronald Phillips, who raped and murdered the 3-year-old daughter of his girlfriend, was supposed to be put to death tomorrow morning. Instead, Gov. John Kasich has postponed the execution until July while the state considers Phillips' plea to donate organs to family members or anyone else who might need them, reports the Columbus Dispatch. "I realize this is a bit of uncharted territory for Ohio, but if another life can be saved by his willingness to donate his organs and tissues then we should allow for that to happen,” said Kasich. If doctors think Phillips' non-vital organs can be harvested, he would undergo surgery before his execution, reports the Cleveland Plain Dealer. This isn't the only reason Phillips' case is making headlines—prison officials plan to use an untested combination of drugs because of a shortage of the standard pentobarbital.


A heroic 11-year-old boy died after he jumped into a frozen Queens pond to save the life of his 12-year-old pal who had fallen through ice, authorities said.

 The deadly accident happened as Anthony Perez, 11, and Juan Umpierrez, 12, were playing in Forest Park at about 4 p.m., officials said.

 “He was on land, he only went out to the ice after the other kid fell through,” a law enforcement source told The Post.

 “He [Perez] was able to push him [Umpierrez] out to safety, but he fell through ice and he couldn’t get out.”

 Rescuers waded through the frigid, chest-high water — whacking a thin layer of ice with their hands — and plucked Perez from the pond, FDNY deputy chief George Healy said.

 But when they got Perez to dry land, he wasn’t breathing — so paramedics performed CPR and rushed the youngster to Jamaica Hospital, where he was pronounced dead.

 “He did help get him out, but he couldn’t save himself,” the law-enforcement source said.

 Perez’s neighbors in Middle Village were shocked and saddened by the news — but not surprised Anthony was so quick to act.

 “I’m going to call him a hero: He’s a hero,” said Carmen Rivera, 51, who lives downstairs from the Perez family.

 “He’s friendly with a lot of people, not shy — he loves to help. He’s a nice little kid.”

 Another neighbor, Leonardo Coraci, 41, also said Perez was well-liked.

 “He’s a good kid, he’s a really great kid . . . it’s a shame something bad had to happen,” said Coraci, who said the pond was once a baseball field.

 “It used to be a baseball field before it was a pond, and they actually had to change it into a stinking pond. They should have kept it as a baseball field. It stinks.

 “He’ll be in my prayers and it’s a shame. He’s a good kid – a really good kid.”

 The FDNY urged parents to warn kids about the dangers of playing on frozen bodies of water in the winter.

 “We implore you: Tell your children, the ice is not safe,” Healy said at a press conference Tuesday. “It’s not gonna support your weight. And there can be tragic consequences.”

 Some of the rescuers fell through the ice themselves while trying to save the boy, he added.

 Two firefighters were also treated for hypothermia.

 “The ice failed underneath them,” Healy said. “They were in chest-deep water. They had to physically break [the ice] with their hands.”

 Days when temperatures reach just above freezing — like on Tuesday when the Big Apple hit 35 degrees — are the most dangerous, Healy said. ||||| "They were in about chest deep water wading through the water. At some point the ice did firm up," Healy said. "They had to physically with their hands break through the ice and chop the ice so they could get to the area they knew that the child would most likely be in, the opening in the ice." ||||| NEW YORK (CBSNewYork) – An 11-year-old boy has died after being pulled from an icy pond Tuesday in Queens.

 First responders were called to Forest Park in Woodhaven around 4:05 p.m. where they found the child unconscious in the water. He was rushed to Jamaica Hospital where he was later pronounced dead.

 As CBS2’s Valerie Castro reported, the victim, identified as 11-year-old Anthony Perez McClean, grew up just minutes away from the pond that claimed his life as he tried to rescue a friend.

 “It doesn’t surprise me at all,” neighbor Angela Vargas said. “Because he’s got a good heart that little boy. Not because I know he’s dead. I can’t do nothing about it.”

 We implore parents – make sure your kids know the ice in the city of New York, on these lakes and ponds, is not safe –#FDNY Deputy Chief Healy from the scene at Forest Park #Queens, where a child was removed from the water after falling through the ice https://t.co/hRjTPmZLHn pic.twitter.com/6CD3T9EyaV — FDNY (@FDNY) February 6, 2018

 Police sources told CBS2 McClean and a 12-year-old friend were near the pond when the older friend walked onto the ice and fell through. McClean walked out to save his friend and fell through the ice himself.

 “It appears that the child went out about 50 feet before the ice let go underneath him and was plunged into the water,” FDNY Dep. Chief George Healy said.

 Police sources said the friend ran home for help, but by the time firefighters arrived, McClean was already submerged and unconscious.

 “They had to – physically with their hands – break through the ice and chop through the ice, so that they could get to the area where they knew the child would most likely be in by the opening in the ice,” said Healy. “They had to go underneath to get the child and remove him.”

 Despite CPR efforts on the scene and on the way to Jamaica Hospital Medical Center, McClean was pronounced dead.

 “It’s a terrible tragedy,” said neighbor Leonardo Coraci. “He’s a good kid, always said ‘hello,’ always respectful.”

 Two firefighters suffered minor injuries.

 “There’s signs around all these lakes in the city. Again, we implore you to tell your children, make sure they’re aware,” Healy said. “Today, the temperature was well above freezing. The ice is not safe, it’s not going to support your weight, and it can have tragic consequences.” |||||
What is a one-paragraph summary of the above article?

– An 11-year-old boy is being called a hero after he died trying to save a friend from a frozen pond Tuesday in New York City. CBS New York reports 11-year-old Anthony Perez and a 12-year-old friend were walking in a park in Queens around 4pm when the friend ventured out onto a frozen pond only to fall through the ice about 50 feet from the shore. Police say Anthony rushed to help his friend and fell in, too. "[Anthony] was able to push him out to safety, but he fell through ice and he couldn’t get out,” a law enforcement source tells the New York Post. The friend immediately ran for help. But by the time firefighters and police officers arrived, Anthony had been underwater for about 30 minutes and wasn't breathing, the New York Daily News reports. Multiple rescuers fell through the ice while trying to get to Anthony. “They had to—physically with their hands—break through the ice and chop through the ice so that they could get to the area where they knew the child would most likely be,” CBS quotes FDNY Deputy Chief George Healy as saying. Rescuers provided CPR at the scene and on the way to the hospital, but Anthony was pronounced dead. Two firefighters had to be treated for hypothermia. A neighbor says it doesn't surprise her that Anthony risked his life to help his friend. "He’s got a good heart that little boy," Angela Vargas says. “I’m going to call him a hero: He’s a hero,” neighbor Carmen Rivera tells the Post. (In Utah, a deputy with no protective gear rescued a boy from a frozen pond.)


Write a summary based on this article:

The crowd gathered at the Conservative Political Action Conference rose to its feet as Chris Christie exited stage left.

 The New Jersey governor, who has been dogged by a scandal stemming from revelations that members of his administration conspired to shut down traffic lanes leading on to the George Washington Bridge, came to CPAC on Thursday in need of a reception like that, and the party faithful delivered.

 Christie’s remarks were highly anticipated, not only because of the lingering scandal but also because CPAC brass dinged him last year by leaving him off of the guest list. Today, the governor was greeted with murmurs and some quiet cheers; he drew more excitement from the audience as he proceeded.

 Currently the chairman of the National Governors Association, Christie used his remarks to praise the work of his colleagues across the country.

 “Republican governors in this country have stood up and done things, not just talked about them,” he said. Praise for Republican governors like Wisconsin’s Scott Walker, Ohio’s John Kasich, and Michigan’s Rick Snyder drew cheers from the crowd.

 Christie returned to a familiar theme, contrasting the labor of the GOP’s governors with the fecklessness of politicians in Washington. “The most dangerous ten feet in Washington, D.C., is between anybody who wants to talk about something and a camera,” he said.

 As Republicans across the country campaign against Obamacare in advance of November’s midterm elections, the governor urged them to hit some positive notes, too. The GOP, he said, is for entrepreneurship and innovation and against the “cold, hard hand of government.” The party supports a strong national defense rather than “one that allows other countries to run us over all over the world.”

 Speaking to an audience that stands to his right, Christie concluded on a cautionary note, tacitly suggesting that the GOP has hurt itself by nominating candidates that are too conservative.

 “We don’t get to govern if we don’t win,” he said. “Let’s come out of this conference resolved to win elections again.” |||||

 Humbled by a scandal that has hampered his rise on the national stage, New Jersey Governor Chris Christie sought to reconnect with the Republican base on Thursday, delivering an uncharacteristically low-key speech to GOP activists that sounded traditional conservative themes.

 “You know I’m shy and retiring, and I don’t like to speak my mind,” Christie joked during his speech at the Conservative Political Action Conference, an annual confab held at a convention center on the banks of the Potomac River outside Washington.

 But the reference to his swaggering image seemed to invoke a figure who wasn’t there. Christie’s remarks were neither brusque nor stirring. He courted the crowd by ticking off familiar tropes, reminding skeptical conservatives of his anti-abortion bona fides and his record of taking on public-sector unions and instituting budget reforms. The Garden State governor assailed the media for bias, cast Democrats as “the party of intolerance,” and urged the GOP to define itself as the party of ideas.

 “Our ideas are better than their ideas,” Christie told the packed ballroom. “We have to stop letting the media define who we are and what we stand for.”

 Christie framed himself as a conservative who has secured a governing majority in a reliably blue state. If the GOP can win in New Jersey, he said, it can borrow the blueprint to expand the political map in coming elections.

 “Governors are about getting things done,” Christie said, lumping himself in with a passel of conservative executives leading blue and purple states, while distancing himself from Washington lawmakers. “Republican governors in this country have stood up and done things — not just talked about them.”

 Christie’s remarks, which lasted about 15 minutes, were a far cry from the all-about-me message he delivered at the 2012 Republican National Convention. His speech Thursday earned a polite reception from the crowd and was punctuated by several rounds of applause. He spoke off the cuff, using notes instead of a teleprompter.

 But his very attendance is a sign that the frost between Christie and his party’s base has thawed. Christie addressed the group in 2012 but did not receive an invitation to CPAC last year. The snub came just months after his public embrace of President Barack Obama in the aftermath of Hurricane Sandy. Many Republicans believed Christie’s effusive praise of the President in the final days of Obama’s re-election campaign helped lift the President over GOP nominee Mitt Romney. Christie spent much of 2013 focused on appealing to his state’s Democrats in order to run up the score of his re-election in preparation for a 2016 presidential campaign.

 The reception may have reflected the media onslaught buffeting Christie, who has been under fire in recent months amid revelations that aides initiated a traffic jam in an apparent act of political retribution. The harsh spotlight from a media conservatives see as biased has earned him new affection from the right.

 Working a crowd that has not always been friendly to his brand of Northeast conservatism, Christie sought to mend fences. He defended the political activity of the billionaire Koch brothers, whose spending on 2014 races has become a rallying cry for vulnerable Senate Democrats. He urged conservatives to stress an economic platform that can lift Americans out of poverty. And he lambasted Obama for standing on the sidelines when Washington required leadership.

 “Mr. President,” he said, “what the hell are we paying you for?” ||||| New Jersey Gov. Chris Christie was his pugnacious self at the Conservative Political Action Conference, giving plenty of red meat and conservative lines to the crowd. In an implicit argument against future political opponents, he said that politicians in Washington just talk but that “Governors are about getting things done.” He blasted those who “stand on the sidelines and spitball,” and he made the case that Republicans must “talk about what we are for, not what we’re against.” There is the message for every governor running against every senator for the GOP presidential nomination. Instead, he argued that conservatives must be confident that “our ideas are better than their [Democrats'] ideas.” He proceeded to reel off accomplishments of several GOP governors in contrast to the “dysfunction” in Congress.

 This was also a speech to remind attendees that he is conservative — pro-market and pro-life. He recounted his budget cuts ($2 billion less in spending than in 2008). Pointing to some diversity of views on abortion in the GOP he declared, after describing a reporter questioning the GOP position on abortion as intolerant, “They’re the party of intolerance, not us.” He, like others, carried a message of “opportunity,” deriding the president’s income-inequality focus in favor of “opportunity inequality.” That is an intriguing theme that deserves further detail. He even defended the Koch brothers, decrying Sen. Harry Reid’s attack on two hardworking Americans!

 Interestingly, he also used the media feeding frenzy at home to boost his conservative street cred, declaring that the GOP should not allow the “media to define us.” Implicit in that is the challenge not to let the mainstream media pick the party’s nominee.

 Christie also took a rare foray into foreign policy, arguing in favor of “America being a leader in the world” and “a strong national defense . . . Not [a country] that allows us to get pushed around all over the world.” That, in a nutshell, is how President Obama is unifying the GOP on national security.

 Christie is still an impressive speaker who knows how to hold a room’s attention. If he is no longer the GOP front-runner, neither can he be ignored in 2016. |||||

– Chris Christie got back in the national spotlight in a way he prefers today—as a featured speaker at the annual CPAC convention for conservatives. The New Jersey governor took particular aim at the media ("We've got to stop letting the media define who we are and what we stand for") and President Obama ("Man, that's leadership, isn't it?"), reports Politico. He also advised members of the GOP and the Tea Party that it's time to "start talking about what we're for and not what we're against." The AP called it an "aggressive message," and Jennifer Rubin at the Washington Post writes that he was back to his "pugnacious self," but the sentiment wasn't unanimous. Time says the "humbled" governor delivered an "uncharacteristically low-key message." Either way, the crowd seemed to warm up to Christie as he went along and rewarded him with a standing ovation at the end, writes Eliana Johnson at the National Review. Rubin sums up: "Christie is still an impressive speaker who knows how to hold a room’s attention. If he is no longer the GOP front-runner, neither can he be ignored in 2016."


Article:

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 Two men were in custody Sunday after a day-long manhunt in Wyoming in connection with the alleged kidnapping and assault of a Utah woman and her four daughters.

 Dereck James "D.J." Harrison, 22, was found and arrested without incident Saturday night after the manhunt in the Half Moon Lake area northeast of Pinedale, Wyoming, police said Sunday.

 His father, Flint Wayne Harrison, 51, had turned himself in to authorities in Sublette County early Saturday. At that point, he "immediately started working with local investigators to locate his son Dereck," county police said in a release.

 Flint and Dereck Harrison in arrest photos in Wyoming on Saturday Sublette County, Wyoming, Sheriff's Office via Centerville, Utah, police

 The Harrisons had been wanted for allegedly luring the mother and her daughters, ages 13 to 18, to a Utah home Tuesday for a barbecue. There, the men allegedly tied them up with wire and duct tape, according to police in Centerville, north of Salt Lake City.

 The woman and some of the young girls were assaulted with a baseball bat as they tried to break free, Centerville police said. But the girls managed to break free and run from the house screaming for help, and one of them called 911 on her cell phone.

 But by the time police arrived, the suspects had already fled.

 Centerville police said Dereck Harrison was believed to have extensively used methamphetamine and may have believed — falsely, it turns out — that the woman had turned him in.

 "The motive appears to be retaliation on the mother," police said Sunday.

 The manhunt centered on Half Moon Lake Lodge in Pinedale, where authorities found a makeshift campsite. Authorities, who said Flint Harrison owns a home in Pinedale, evacuated the campground Saturday and urged the town's 2,000 residents to shelter in place.

 Flint Wayne Harrison, left, and Dereck James Harrison. Centerville, Utah, police / AP

 The Sublette County Sheriff's Office said the younger Harrison was believed to have been armed with two knives, a 300 Winchester Magnum rifle, a .22-caliber Remington rifle and several high-capacity magazines. Authorities said he had made several threats against law enforcement officials.

 Deputies found him walking a little more than a mile from a roadblock. "This is an incredible end to a very stressful day,” Sheriff Stephen Haskell said in a statement.

 Both father and son will be extradited to Utah to face charges, according to the Sublette County Sheriff's Office.

 It is unclear whether they will face additional charges in Wyoming, where the elder Harrison is registered as a sex offender for attempted forcible sexual abuse in 2001, according to the Wyoming Division of Criminal Investigation. ||||| Starting in 1996, Alexa Internet has been donating their crawl data to the Internet Archive. Flowing in every day, these data are added to the Wayback Machine after an embargo period. |||||
What is a summary?

– A 22-year-old man and his parents have been arrested after the alleged abduction of a woman in Utah and her four teen daughters. The latter five managed to escape and alert authorities, reports NBC News. Police say Dereck Harrison, 22, and his father, Flint Harrison, 51, knew the Utah mother and suspected her of telling authorities about their drug use. They lured her and her daughters, ages 13 to 18, to a home on the pretext of a barbecue, then tied all five up with zip ties, say police. The elder Harrison hit the mother with a baseball bat, at which point the daughters began breaking free from their ties, say the charging documents, per the Casper Tribune. One of the girls knocked away a shotgun pointed at her throat and another seized the bat and hit the younger Harrison with it, say police. The victims fled, as did the Harrisons, but both suspects eventually surrendered separately in Wyoming and now face charges of aggravated kidnapping and possession of a controlled substance. While Dereck Harrison was still on the loose, his mother, Maryann Dalrymple Harrison, went to police in Wyoming to obtain information about her son, but she, too, ended up under arrest. It seems she violated her probation by leaving Utah without permission. (No more details were provided on her case.) Police say that the victims are recovering but that the Harrisons aren't cooperating with the investigation.


Here is a news article: Organisers of the Emmy Awards managed to annoy thousands of viewers after creating a montage of spoilers for hit television shows.

 While finales are often revealed on social media, it is unlikely that boxset fans were expecting the industry's biggest awards ceremony to ruin things for them.

 The film contained the endings to shows such as Nurse Jackie, Boardwalk Empire, Sons Of Anarchy and Mad Men.

 Host Andy Samberg was quick to acknowledge that many people would be upset about the spoilers.

 "Welcome back to the spoiler awards. I guess everyone on every show died," he said after a break.

 1 / 16 Gallery: US Stars Triumph At Emmy Awards The cast and crew of Game Of Thrones were honoured with the best drama series prize

 Unsurprisingly there was some anger on Twitter.

 Dalton Ross tweeted: "The #Emmys just set the land-speed record for most spoilers per minute."

 "That whole #Emmys montage celebrating shows that have ended was just a series of spoilers for anyone who hasn't finished any of those shows," wrote user Ashley Renee.

 But there was a lack of sympathy from some who highlighted that many of the shows ended earlier this year and had been talked about widely on the internet.

 Kelly Sharon tweeted: "To everyone complaining about spoilers: most of those shows ended in the spring. If you haven't watched you're not going to."

 Mad Men star Jon Hamm walked away with the lead actor prize at the Microsoft Theatre after an eight-year wait. ||||| A horde of fans was left feeling shocked and betrayed at last night's Emmys after a video montage revealed a series of spoilers for many of the shows that ended this year.

 Viewers were left dumbfounded as revealing clips from "Mad Men," "Boardwalk Empire" and "Parenthood" infiltrated their TVs – with many complaining they'll now never be able to watch those shows with the unwitting mentality they deserve.

 The montage also showed revealing clips from "Boardwalk Empire." (HBO/Christopher T. Saunders)

 JON HAMM FINALLY WINS FIRST EMMY AFTER 7 LOSSES

 "Thanks for the series finale spoilers in that montage #Emmys2015," tweeted user Derick Valadao. "Brutal."

 I can't believe The Emmys just gave away so many spoilers in that memoriam. — Gideon Glick (@gidglick) September 21, 2015

 Hey #Emmys, we aren’t all @AndySamberg! Not everyone can lock themselves in a bunker and watch ALL the shows. #spoilers — Donna Dickens (@MildlyAmused) September 21, 2015

 Thx for all the spoilers, Emmys. Jeez. — Matt Miller (@Official_MattM) September 21, 2015

 Thanks, #Emmys for the devastating spoilers package — Scott Lamica (@Slamica) September 21, 2015

 "I mean seriously how f------ stupid are the people who put together that montage of spoilers?" another user named Joshua Topolsky said.

 Emmys host Andy Samberg only added insult to injury to the seething fans, as he jokingly pointed out that the montage obviously unveiled critical scenes from the ends of the shows.

 "Welcome back to the Spoiler Awards," Samberg quipped after the montage.

 At the beginning of the show, Samberg starred in a pre-recorded musical number where he sang about locking himself in a bunker for a year so he could binge watch every TV series out right now.

 But evidently, not everyone had that luxury of time.

 "Hey #Emmys, we aren't all @AndySamberg!" tweeted user Donna Dickens. "Not everyone can lock themselves in a bunker and watch ALL the shows."

 The Emmys did have a few brave supporters, however.

 "To everyone complaining about spoilers: most of those shows ended in the spring," tweeted Kelly Sharon. "If you haven't watched you're not going to."

 They probably would've at least liked the chance to watch them, though.

 More stories from the 2015 Emmys:

 Andy Samberg's top ten jokes from the Emmys opening monologue

 Five things you should know about 'Olive Kitterige' after big Emmy wins

 Emmys' 2015 big winners are 'Game of Thrones,' Jon Hamm and Viola Davis; Tracy Morgan makes emotional appearance |||||
A summary of this is?

– Whoops: Viewers watching the Emmys last night were dismayed when a montage celebrating shows that came to a close this year gave away the endings of many of those shows, Sky News reports. Among the series spoiled: Mad Men, Sons of Anarchy, Nurse Jackie, Parenthood, and Boardwalk Empire. "Welcome back to the spoiler awards," host Andy Samberg said when he came back onstage. "I guess everyone on every show died." There was outrage on Twitter, the New York Daily News reports, but not everyone was sympathetic to the complainers. For example: "To everyone complaining about spoilers: most of those shows ended in the spring. If you haven't watched you're not going to," tweeted one person. But, as another pointed out, "Hey #Emmys, we aren’t all @AndySamberg! Not everyone can lock themselves in a bunker and watch ALL the shows."


Article:

The seed for this crawl was a list of every host in the Wayback Machine

 This crawl was run at a level 1 (URLs including their embeds, plus the URLs of all outbound links including their embeds)

 The WARC files associated with this crawl are not currently available to the general public. ||||| As you may have heard, Goldman Sachs is being sued for fraud by the Securities and Exchange Commission for allegedly misleading investors about a deal that Goldman helped structure and sell. In the civil suit, the SEC specifically faulted Goldman for failing to disclose that a hedge fund was helping create the investment while betting big the deal would fail.

 According to the SEC, Goldman Sachs knew about the hedge fund’s bets, knew it played a significant role in choosing the assets in the portfolio, and yet did not tell investors about it. (Goldman Sachs has called the SEC’s accusations “completely unfounded in law and fact.” And in another more detailed statement, it said it “did not structure a portfolio that was designed to lose money.”)

 As we reported at ProPublica last week, many other major investment banks were doing a similar thing.

 Investment banks including JPMorgan Chase, Merrill Lynch (now part of Bank of America), Citigroup, Deutsche Bank and UBS also created CDOs that a hedge fund named Magnetar was both helping create and betting would fail. (Update 4/17: Magnetar denies it was making such bets.) Those investment banks marketed and sold the CDOs to investors without disclosing Magnetar’s role or the hedge fund’s interests.

 Here is a list of the banks that were involved in Magnetar deals, along with links to many of the prospectuses on the deals, which skip over Magnetar’s role. In all, investment banks created at least 30 CDOs with Magnetar, worth roughly $40 billion overall. Goldman’s 25 Abacus CDOs—one of which is the basis of the SEC’s lawsuit—amounted to $10.9 billion.

 Our reporter Jake Bernstein explained the investment banks’ disclosure failures on Chicago Public Radio’s “This American Life”:

 The role of Magnetar, both as equity investor and in their bets against the very CDOs they helped create, were not disclosed in any way to investors in the written documents about the deals. Not the marketing materials, not the prospectuses, not in the hundreds of pages that an investor could get to see information about the deal was it disclosed that it was in fact Magnetar who’d helped create the deal, and who’d bet against.

 That is, of course, along the lines of what the SEC is suing Goldman Sachs for now. The SEC’s suit also says CDOs like the ones Goldman built “contributed to the recent financial crisis by magnifying losses associated with the downturn in the United States housing market.”

 Notably, the SEC did not sue the hedge fund involved in Goldman’s Abacus deals—Paulson & Co.—or its manager, John Paulson. Instead, it’s going after Goldman. And as we pointed out in our reporting, there’s no evidence that what Magentar did was illegal.

 We’ve called the major banks involved in Magnetar CDO deals to see if they were concerned about similar lawsuits. Thus far, Bank of America, Citigroup, Deutsche, Wells Fargo (which bought Wachovia) and UBS have responded and have all declined our requests for comment. Here is Magnetar’s response to our original reporting.

 Read ProPublica’s full Magnetar story.

 ProPublica’s Ryan Knutson contributed to this report. |||||
What is a summary?

– The SEC's fraud suit against Goldman Sachs might be just the tip of the iceberg, because other investment banks engaged in exactly the same sleight of hand, Pro Publica reports. Goldman is accused of failing to disclose that a hedge fund was both helping to create, and betting against, the investments Goldman was selling. But several other investment banks, including JPMorgan Chase, Merrill Lynch and Citigroup all did the same thing. The SEC is already investigating some of these other deals, the Wall Street Journal adds. The agency says it'll sue if it believes banks misrepresented securities to their clients. Indeed, Rabobank already sued Merrill Lynch last year, alleging that Merrill did just that with some securities that the hedge fund Magnetar helped create and bet against. When the Goldman case came out, Rabobank issued a statement saying it was “the same type of fraudulent conduct” Merrill had engaged in.


When Americans sit down with their families for Thanksgiving dinner, most of us will probably gorge ourselves on the same traditional Thanksgiving menu, with turkey, cranberry sauce, stuffing, and pumpkin pie taking up the most real estate on our plates. How did these dishes become the national "what you eat on Thanksgiving" options, though?

 The pilgrims may not have had turkey

 Turkey may not have been on the menu at the 1621 celebration by the pilgrims of Plymouth that is considered the first Thanksgiving (though historians and fans of Virginia's Berkeley Plantation might quibble with the "First" part). There were definitely wild turkeys in the Plymouth area, as colonist William Bradford noted in his journal. However, the best existing account of the pilgrims' harvest feast comes from colonist Edward Winslow, author of Mourt's Relation: A Journal of the Pilgrims at Plymouth. Winslow's first-hand account of the first Thanksgiving included no explicit mention of turkey. He does, however, mention the pilgrims gathering "wild fowl" for the meal, although that could just as likely have meant ducks or geese.

 So why do we chow down on turkey, then?

 It helps to know a bit about the history of Thanksgiving. While the idea of giving thanks and celebrating the harvest was popular in certain parts of the country, it was by no means an annual national holiday. Presidents would occasionally declare a Thanksgiving Day celebration, but the holiday hadn't completely caught on nationwide. Many of these early celebrations included turkey; Alexander Hamilton once remarked that, "No citizen of the U.S. shall refrain from turkey on Thanksgiving Day."

 When Bradford's journals were reprinted in 1856 after being lost for a century, they found a receptive audience with advocates who wanted Thanksgiving turned into a national holiday. Since Bradford wrote of how the colonists had hunted wild turkeys during the autumn of 1621 and since turkey is a uniquely American (and scrumptious) bird, it gained traction as the Thanksgiving meal of choice for Americans after Lincoln declared Thanksgiving a national holiday in 1863.

 Moreover, there were pragmatic reasons for eating turkey rather than, say, chicken at a feast like Thanksgiving. The birds are large enough that they can feed a table full of hungry family members, and unlike chickens or cows, they didn't serve much utilitarian purpose like laying eggs or making milk. Unlike pork, turkey wasn't so common that it didn't seem like a suitable choice for a special occasion, either. An interesting 2007 piece in Slate discussed these reasons for turkey's prominence, but also made another intriguing point. The publication of A Christmas Carol in 1843 may have helped force along the turkey's cause as a holiday delicacy when Scrooge magnanimously sends the Cratchit family a Christmas turkey.

 There was no cranberry sauce, either

 While the cranberries the pilgrims needed were probably easy to come by, making cranberry sauce requires sugar. Sugar was a rare luxury at the time of the first Thanksgiving, so while revelers may have eaten cranberries, it's unlikely that the feast featured the tasty sauce. What's more, it's not even entirely clear that cranberry sauce had been invented yet. It's not until 1663 that visitors to the area started commenting on a sweet sauce made of boiled cranberries that accompanied meat. There's the same problem with potatoes. Neither sweet potatoes nor white potatoes were available to the colonists in 1621, so the pilgrims definitely didn't feast on everyone's favorite tubers.

 They did have plenty of venison, though

 Winslow mentions in his writings that the governor sent out a party of four men to do some fowling for the feast, but the pilgrims and Wampanoag also enjoyed five deer as part of their feasting. The meat supposedly arrived at the celebration as a gift from the Wampanoag king Massasoit. On top of the venison, other meats probably included lots of fish and shellfish, which were staples of the pilgrims' diets. So if you want to wolf down a lobster or some oysters in lieu of turkey on Thursday, nobody can fault you for being historically inaccurate.

 And pumpkin pie didn't cap things off

 It may be the flagship dessert at modern Thanksgiving dinners, but pumpkin pie didn't make an appearance at the first Thanksgiving. The pilgrims probably lacked the butter and flour needed to make a pie crust, and it's not clear that they even had an oven in which they could have baked a pumpkin pie. That doesn't mean pumpkins weren't available for the meal, though; they were probably served after being baked in the coals of a fire or stewed. Pumpkin pie became a popular dish on 17th-century American tables, though, and it might have shown up for Thanksgiving as early as the 1623 celebration of the holiday.

 More from Mental Floss... ||||| Every schoolchild learns that the Pilgrims couldn't have survived life in the New World without the help of the Indians. The tribes taught them which crops to plant. They introduced them to corn and other nutritional mainstays. One of these, the American cranberry, is still part of the classic Thanksgiving feast. (See more photos of cranberries.)

 What you probably don't know, though, is that the cranberry was a key ingredient in the original energy bar, 400 years before anyone knew what a superfood was.

 The Algonquin, Chippewa, and Cree, among others, gathered wild cranberries where they could find them in what is now Maine, Massachusetts, New Jersey, and Wisconsin, all the way west to Oregon and Washington, and north to areas of British Columbia and Quebec, according to Devon Mihesuah, a professor at the University of Kansas and an enrolled citizen of the Choctaw Nation. The berry was called sassamenesh (by the Algonquin) and ibimi (by the Wampanoag and Lenni-Lenape), which translates literally as "bitter" or "sour berries." Cranberries were used for everything from cooking to dyes for textiles to medicines.

 According to Mihesuah, who also runs the American Indian Health and Diet Project, the Native Americans ate cranberries as fresh fruit, dried the fruit and formed them into cakes to store, and made tea out of the leaves. The Inuktitut of eastern Canada used the cranberry leaves as a tobacco substitute. There were also a range of nonculinary uses for the berry, says Mihesuah. Cree boiled the fruit and used it to dye porcupine quills for clothing and jewelry. Chippewa used cranberries as bait to trap the snowshoe hare.

 And harnessing the nutritional power of the fruit—cranberries are extremely high in antioxidants and are thought to help prevent heart disease—Iroquois and Chippewa used cranberries for an assortment of medicinal purposes: as "blood purifiers," as a laxative, and for treating fever, stomach cramps, and a slew of childbirth-related injuries.

 Pemmican—the Original Energy Bar

 One of the more intriguing ways the Indians prepared cranberries was in a mixture called pemmican—sort of like a modern-day energy bar. They would pound cranberries into a mixture of equal parts ground dried deer meat and fat tallow, then store the mixture in animal skin pouches. "The fat preserves it, as does the acidity in the fruit, which lowers the pH and helps resist bacteria," says food historian Ken Albala, of University of the Pacific. The pemmican would last for months and could be eaten on long journeys as a reliable source of protein and fat.

 Pemmican was essential to the Indians and Europeans engaged in the fur trade. For the traders, pemmican was a chief source of calories on the winter trade routes; for the Métis Indians, pemmican was a source of commerce.

 "So vital was pemmican to the survival of fur traders and early settlers in Canada," writes food historian and cookbook author Jennifer McLagan, "that its supply sparked unrest between the Native Americans and the Europeans." Responding to a food shortage in 1814, the governor of the Red River colony, Miles Macdonell, attempted to prohibit the export of pemmican by the Métis. The Métis reacted by banding together with fur traders and, in 1816, they attacked the Red River settlement, in a clash known today as the Battle of Seven Oaks.

 Cranberries and the Colonists

 In all likelihood, the American cranberry was completely new to the European settlers, who came mostly from southern England. "Certainly there are cranberries in Great Britain, so the colonists may have had a frame of reference for it," says Stephen Cole, author of The Cranberry: Hard Work and Holiday Sauce. "The cranberry that became the cultivated cranberry that's harvested and eaten today is distinctive to North America, though."

 The colonists had a few names for the cranberry: Craneberries, for the way the flower, produced in early June before the fruit grows, resembles the head and bill of a sandhill crane; fenberries, for the fens—an antiquated word for bogs—where cranberries grow; and bearberries, for the bears that were, apparently, often seen snacking on them.

 But the colonists were indifferent to the Indians' wide range of uses for the cranberry. In fact, they were mostly adapting the fruit to fit the recipes and uses they knew from the Old World. "They were using cranberries in a medieval culinary tradition," says Cole. "Colonists never ate anything like pemmican within the tradition they had, which was mostly stuffings and puddings." Food historian Albala agrees: "The Europeans used cranberries the way they would have used similar fruits ... as a sour fruit sauce with wild fowl."

 Sweetening the Deal

 In 1622, the British brought honeybees to North America, changing the ways the colonists could use the fruit. "Once there was a consistent form of sweetening," says Cole, "the cranberry takes off. It gets used as a slightly tart side dish and ends up in pies and tarts." Soon, it's featured on the tables of high society. William Tudor, a satirist and well-known figure among Boston society in the early 19th century, wrote mockingly of cranberry sauce that it "is eaten with almost every species of roasted meat, particularly the white meats, turkies, &c. Some even eat it with boiled fish, and I knew one person, otherwise a very worthy man, who eats it with lobsters, for supper!"

 By the mid-19th century, when the European settlers began formally cultivating the cranberry for commercial use, the Indians were gone. "Tribes were pretty well wiped out within a hundred years of contact in New England," says Mihesuah. "They had a heck of time just surviving, and if they did manage to cultivate cranberries to any extent, it did not last long."

 The cranberry industry that began over 250 years ago has thrived, and today is worth over $300 million. (Watch "Cranberry Harvest" at Wisconsin's oldest cranberry marsh.)

 There are independently owned cranberry farms across the northern United States and southern Canada—and some Indian tribes have kept their connection to the berry. An organic cranberry farm in Oregon, Coquille Cranberries, is owned and operated by members of the Coquille tribe. And each year, on the second Tuesday in October, the Wampanoag celebrate Cranberry Day on Martha's Vineyard. ||||| “It is indeed bad to eat apples. It is better to make them all into cider”

 —Benjamin Franklin, in Remarks Concerning the Savages of North America, reporting an American Indian’s response to hearing the story of Adam and Eve.

 No one knows exactly what the Pilgrims drank at the first Thanksgiving back in 1621. No known televised documentaries have survived to date, and little written documentation chronicling the meal exists. However, all evidence points to the fact that the Pilgrims toasted survival and that first harvest in America with mugs of hard apple cider.

 Cider became a staple in England during the 16th and 17th centuries, dubbed the beverage’s “Golden Age.” While the drink had existed in initial forms for centuries, cider’s influence remained relatively contained to England’s upper crust (they had ample time and money to cultivate orchards) until the end of the 16th century, when it became a more democratic tipple.

 Cider’s history, like the apple’s is long, curious, and celebrated. The cultivated apple we know today is the Malus pumila or M. Domestica and most likely originated in the Tien Shah Mountains, along the border between northwest China and Kazakhstan. (Kazakh capital’s name, “Alma-Ata,” means “father of apples.”) That apple probably derived from the M. Sieversii, which grows wild in a number of places, making the apple’s origin especially hard to pin down. In his book Cider: Hard and Sweet, Ben Watson notes that wild apples are depicted on Paleolithic cave art that dates back as far as 30,000 BCE. Around 8,000 years ago, apples began to surface in trade routes and began to pass through Central Asia. Homer writes of them in The Odyssey, and apples were Alexander the Great’s favorite dessert.

 Cider’s birthplace is nearly as hard to identify, though the first record of cider production dates back to Rome. Julius Caesar and his soldiers drank cider made from crabapples in 55 BC. Throughout their conquests, Romans brought apple cuttings and horticultural knowledge across Europe (including to England), and by the 2nd Century CE, Romans were making cider (they called it “apple wine”), which we can read all about thanks to Pliny the Elder.

 In 1066, after a long lull in cider production, the Norman Conquest (led by William II of Normandy, who became William the Conqueror) sparked a renewed cider interest in England. William’s army brought cuttings of several varieties including the Pearmain (a pear) among others. Cider soon became the most popular drink after ale and gained new ground again in the early 16th century, when Richard Harris (“fruiterer” to Henry VIII) procured several additional apple grafts from France, including Pippins, a desert apple that made sweet and delicious ciders.

 England’s growing shipping trade during the 16th and 17th Centuries also contributed to cider’s increasing demand. Ted Bruning notes in Golden Fire: The Story of Cider, that the English soon realized “a sealed cask of cider…will not only keep but will go on improving for months or even years.” Sea captains observed that fewer passengers contracted scurvy on ships stocked with casks of cider aboard. Bruning also records that cider’s acclaim grew after several brutally cold winters wiped out vineyards in England and along France’s west coasts. Two additional factors spurred cider’s growing popularity at the time: trade restrictions on ale (which did not exist on cider) and England’s shortage of burnable wood (which impeded ale production).

 During the middle of this Golden Age, in 1620, the Pilgrims landed at Plymouth Rock. Several species of apples grew native in the area (garland, sweet crab, prairie crab, and southern crab), making it likely that the Pilgrims brewed their own cider, and American-bound English ships would have provided a steady supply as well. Early settlers used the apple cider for a variety of other products including applejack (initially produced by settlers who left buckets of fermenting cider out in the cold, then removed the layer of accumulated ice), apple brandy, and cider vinegar. Apple trees spread as settlers did, and by 1775, one in every ten farms in New England operated a cider mill. (Water was either unpalatable or, near towns, polluted, ale grew increasingly expensive and early attempts at growing barley and hops failed miserably.) According to Watson, by 1767 cider consumption per-capita had reached 1.14 barrels—more than 35 gallons per person.

 Then beer became America’s favorite beverage, a position it still holds today. But cider production and consumption is on the rise after a long fallow period. In the United States, demand for cider has increased 65 percent in the past two years alone, far outpacing craft beer and wine.

 In the spirit of historical tradition, cider would make an excellent addition to any Thanksgiving meal. Cider boasts acidity and (generally) effervescence, both of which cleanse the palate and add brightness and lift to rich dishes. In addition, cider is lower in alcohol than wine or beer, and it usually hovers at around five percent alcohol by volume. This makes it an excellent beverage to sip while you’re preparing Thanksgiving dinner, too.

 In case you are not all that familiar with cider, here are a few rules of note – in extremely generalized terms that will probably get me in trouble. Ciders from France taste like apples (or pears). Ciders from Spain taste like feet. Ciders from America are a little bit boring (but getting better).

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 What does that mean? In Normandy, French cider makers – especially top producers like Eric Bordelet, Etienne Dupont, and Cyril Zangs, are making ciders that are sweet, fragrant, and taste of fruit. Bordelet worked for years as a sommelier at l’Arpege, in Paris, and his ciders in particular behave like refined wines. They are nuanced and pure. Dupont's are slightly more rustic but equally magical. Zangs’ are lively and pure, and slightly spicy and herbaceous.

 In Asturias, the cider apples are more bitter and tannic than in other regions. The style they produce resembles sour ale more than fruit. Isastegi Cider is one of the region’s most classic and elegant. In Asturias, more cider is consumed per capita than anywhere else in the world.

 In America, we are finally rediscovering our cider-loving roots. Unfortunately, most heirloom apple trees have long since been ripped out of the ground. Trees have been replanted, but we will have to wait a few years until those trees mature. Foggy Ridge Cider, in Virginia, is making clean and bright ciders. Aaron Burr Cidery in Wurtsboro, New York, makes tiny quantities of funky, interesting cider from heirloom varieties, fermented with indigenous yeasts.

 With a history that includes the Pilgrims, Julius Caesar, William the Conqueror (not to mention Charlemagne, who planted orchards in 800 CE), among others, cider’s renaissance is a welcome return to American roots. In the name of history and deliciousness, it is especially welcome this year at my Thanksgiving table. |||||

Write a summary.

– The pilgrims may not have eaten any turkey at the "First Thanksgiving" in 1621—no mention of turkey is specifically mentioned in Edward Winslow's account of the feast, but he does mention that a lot of venison was eaten, and they probably ate fish and shellfish as well—so why is it the traditionally accepted main course for Thanksgiving today? Well, the Week explains, William Bradford's journals were rediscovered and reprinted in 1856, and he wrote about the wild turkey hunts the colonists engaged in in 1621. Plus, turkey is a very American bird, and a large enough one to feed a table full of people, so when Abraham Lincoln officially made Thanksgiving a national holiday in 1863, that's what was on the menu. The pilgrims didn't eat cranberry sauce, either, considering sugar was a luxury at the time and it's kind of an integral ingredient in the sauce. (They may have eaten plain cranberries, though; National Geographic notes that the fruit was a sort of Native American "superfood.") And neither sweet potatoes nor white potatoes were around in America quite yet, so those weren't on the menu either, nor was pumpkin pie—since the pilgrims probably didn't have the butter or flour they would have needed to make the crust. If you'd like to be historically accurate at least when it comes to the beverages, the pilgrims probably drank hard apple cider, the Daily Beast reports.