den lille pige
med svovlstikkerne
(the little match girl)
sugar
fat chance: beating the odds against sugar, processed food, obesity, and disease
robert lustig 2013 9781594631009
sugar rush or sugar crash? a meta-analysis of carbohydrate effects on mood
konstantinos mantantzis et al. 2019
doi.org/10.1016/j.neubiorev.2019.03.016
•Carbohydrates do not have a beneficial effect on any aspect of mood.
•Carbohydrate consumption lowers alertness within 60 minutes after consumption.
•Carbohydrates increase fatigue within 30 minutes post-consumption.
The effect of carbohydrate (CHO) consumption on mood is much debated, with researchers reporting both mood improvements and decrements following CHO ingestion. As global consumption of sugar-sweetened products has sharply increased in recent years, examining the validity of claims of an association between CHOs and mood is of high importance. We conducted a systematic review and meta-analysis to evaluate the relationship between acute CHO ingestion and mood. We examined the time-course of CHO-mood interactions and considered the role of moderator variables potentially affecting the CHO-mood relationship. Analysis of 176 effect sizes (31 studies, 1259 participants) revealed no positive effect of CHOs on any aspect of mood at any time-point following their consumption. However, CHO administration was associated with higher levels of fatigue and less alertness compared with placebo within the first hour post-ingestion. These findings challenge the idea that CHOs can improve mood, and might be used to increase the public's awareness that the ‘sugar rush’ is a myth, inform health policies to decrease sugar consumption, and promote healthier alternatives.
the depressogenic potential of added dietary sugars
daniel j. reis et al. 2019
doi.org/10.1016/j.mehy.2019.109421
“For many people, reduced sunlight exposure during the winter will throw off circadian rhythms, disrupting healthy sleep and pushing five to 10% of the population into a full-blown episode of clinical depression,” said Stephen Ilardi, KU associate professor of clinical psychology.
Ilardi, who coauthored the study with KU graduate students Daniel Reis (lead author), Michael Namekata, Erik Wing and Carina Fowler (now of Duke University), said these symptoms of “winter-onset depression” could prompt people to consume more sweets.
“One common characteristic of winter-onset depression is craving sugar,” he said. “So, we’ve got up to 30% of the population suffering from at least some symptoms of winter-onset depression, causing them to crave carbs — and now they’re constantly confronted with holiday sweets.”
Ilardi said avoidance of added dietary sugar might be especially challenging because sugar offers an initial mood boost, leading some with depressive illness to seek its temporary emotional lift.
“When we consume sweets, they act like a drug,” said the KU researcher, who also is author of “The Depression Cure” (First De Capo Press, 2009). “They have an immediate mood-elevating effect, but in high doses they can also have a paradoxical, pernicious longer-term consequence of making mood worse, reducing well-being, elevating inflammation and causing weight gain.”
The investigators reached their conclusions by analyzing a wide range of research on the physiological and psychological effects of consuming added sugar, including the Women’s Health Initiative Observational Study, the NIH-AARP Diet and Health Study, a study of Spanish university graduates, and studies of Australian and Chinese soda-drinkers.
Ilardi cautioned it might be appropriate to view added sugar, at high enough levels, as physically and psychologically harmful, akin to drinking a little too much liquor.
“We have pretty good evidence that one alcoholic drink a day is safe, and it might have beneficial effect for some people,” he said. “Alcohol is basically pure calories, pure energy, non-nutritive and super toxic at high doses. Sugars are very similar. We’re learning when it comes to depression, people who optimize their diet should provide all the nutrients the brain needs and mostly avoid these potential toxins.”
The researchers found inflammation is the most important physiological effect of dietary sugar related to mental health and depressive disorder.
“A large subset of people with depression have high levels of systemic inflammation,” said Ilardi. “When we think about inflammatory disease we think about things like diabetes and rheumatoid arthritis — diseases with a high level of systemic inflammation. We don’t normally think about depression being in that category, but it turns out that it really is — not for everyone who’s depressed, but for about half. We also know that inflammatory hormones can directly push the brain into a state of severe depression. So, an inflamed brain is typically a depressed brain. And added sugars have a pro-inflammatory effect on the body and brain.”
Ilardi and his collaborators also identify sugar’s impact on the microbiome as a potential contributor to depression.
“Our bodies host over 10 trillion microbes and many of them know how to hack into the brain,” Ilardi said. “The symbiotic microbial species, the beneficial microbes, basically hack the brain to enhance our well-being. They want us to thrive so they can thrive. But there are also some opportunistic species that can be thought of as more purely parasitic — they don’t have our best interest in mind at all. Many of those parasitic microbes thrive on added sugars, and they can produce chemicals that push the brain in a state of anxiety and stress and depression. They’re also highly inflammatory.”
abstract Added sugars are ubiquitous in contemporary Western diets. Although excessive sugar consumption is now robustly associated with an array of adverse health consequences, comparatively little research has thus far addressed its impact on the risk of mental illness. But ample evidence suggests that high-dose sugar intake can perturb numerous metabolic, inflammatory, and neurobiological processes. Many such effects are of particular relevance to the onset and maintenance of depressive illness, among them: systemic inflammation, gut microbiota disruption, perturbed dopaminergic reward signaling, insulin resistance, oxidative stress, and the generation of toxic advanced glycation end-products (AGEs). Accordingly, we hypothesize that added dietary sugars carry the potential to increase vulnerability to major depressive disorder, particularly at high levels of consumption. The present paper: (a) summarizes the existing experimental and epidemiological research regarding sugar consumption and depression vulnerability; (b) examines the impact of sugar ingestion on known depressogenic physiological processes; and (c) outlines the clinical and theoretical implications of the apparent sugar-depression link. We conclude that the extant literature supports the hypothesized depressogenic impact of added dietary sugars, and propose that an improved understanding of the effects of sugar on body and mind may aid in the development of novel therapeutic and preventative measures for depression.
fructose-1,6-bisphosphate couples glycolytic flux to activation of ras
ken peeters et al. 2017
doi.org/10.1038/s41467-017-01019-z
pure, white, and deadly: how sugar is killing us and what we can do to stop it
john yudkin 2013 to read next
an exploration of the aversive properties of 2-deoxy-d-glucose in rats
thomas horman et al. 2018
doi.org/10.1007/s00213-018-4998-1
Hypoglycemia can alter arousal and negatively impact mood. This study tests the hypothesis that acute drops in glucose metabolism cause an aversive state mediated by monoamine activity. In experiment 1, male Sprague-Dawley rats were either food deprived (FD) or pre-fed (PF) and tested on conditioned place avoidance (CPA; biased place conditioning design; 3 pairings drug/vehicle, each 30 min-long) induced by the glucose antimetabolite 2-deoxy-d-glucose (2-DG; 0, 300 or 500 mg/kg, SC). Locomotion and blood glucose were also assessed. Experiment 2 examined whether clonidine (noradrenergic α2 agonist, 0, 10 or 40 μg/kg, SC) or bupropion (monoamine reuptake blocker, 0, 10 or 30 mg/kg, SC) could alter CPA induced by 500 mg/kg 2-DG. In experiment 3, blood corticosterone (CORT) was measured in response to 500 mg/kg 2-DG, alone or in combination with 40 μg/kg clonidine or 30 mg/kg bupropion. Finally, experiment 4 controlled for possible place conditioning induced by 10 or 40 μg/kg clonidine, or 10 or 30 mg/kg bupropion injected without 2-DG. It was found that 2-DG increased blood glucose and produced a robust CPA. The feeding status of the animals modulated these effects, including CORT levels. Both clonidine and bupropion attenuated the effects of 2-DG on CPA and CORT, but only bupropion reversed suppression of locomotion. Taken together, these results in rats suggest that impaired glucose metabolism can negatively impact arousal and mood via effects on HPA and monoamine systems.
u.s. obesity as delayed effect of excess sugar
r. alexander bentley et al. 2019
http://dx.doi.org/10.1016/j.ehb.2019.100818
"While most public health studies focus on current behaviors and diets, we took a novel approach and looked at how the diets we consumed in our childhood affect obesity levels now that we are adults," said Alex Bentley, head of UT's Department of Anthropology and lead researcher of the study, which was published in Economics and Human Biology.
Consumption of excess sugar, particularly in sugar-sweetened beverages, is a known contributor to both childhood and adult obesity. Many population health studies have identified sugar as a major factor in the obesity epidemic. One problem with this theory, however, has been that sugar consumption in the US began to decline in the late 1990s while obesity rates continued to rise well into the 2010s.
That increase shows in the numbers: By 2016, nearly 40 percent of all adults in the US -- a little over 93 million people -- were affected by obesity. In Tennessee alone, the adult obesity rate more than tripled, from about 11 percent in 1990 to almost 35 percent in 2016. By 2017, however, obesity in Tennessee had fallen 2 percent from the previous year.
If high-sugar diets in childhood have long-lasting effects, the changes we see now in adult obesity rates may have started with diets decades ago, when those adults were children.
"Since the 1970s, many available infant foods have been extremely high in sugar," said Hillary Fouts, coauthor of the study and cultural anthropologist and professor in the UT Department of Child and Family Studies. "Other independent studies in medicine and nutrition have suggested that sugar consumption during pregnancy can cause an increase in fat cells in children," she added.
"Up to this point, no studies had explicitly explored the temporal delay between increased sugar consumption and rising obesity rates," says Damian Ruck, postdoctoral research fellow in the Department of Anthropology and coauthor of the study. To address the problem, the authors modeled the increase in US adult obesity since the 1990s as a legacy of the increased excess sugar consumption measured among children in the 1970s and 1980s.
The researchers tested their model using national obesity data collected between 2004 and 1990 by the Centers for Disease Control and Prevention. They compared those obesity rates with annual sugar consumption since 1970 using the median per capita rates issued by the US Department of Agriculture.
The model also roughly captures how obesity rates vary by age group among children and teenagers.
"Our results suggest that the dietary habits learned by children 30 or 40 years ago could explain the adult obesity crisis that emerged years later," said Ruck.
A large portion of the sugar increase before 2000 was from high fructose corn syrup (HFCS), which after 1970 quickly become the main sweetener in soft drinks and a common ingredient in processed foods. At peak sugar consumption, in 1999, each person in the US consumed on average around 60 pounds of HFCS per year and more than 400 calories per day in total excess sugars.
US sugar consumption has declined since 2000. "If 2016 turns out to be the peak in the obesity rate," Bentley added, "that is coincidentally one generation after the peak in excess sugar consumption."
The researchers are planning to continue their studies in the area by exploring the effect of sugar-sweetened beverages. "This is important because obesity disproportionately affects the poor," said Bentley.
In a paper published in Palgrave Communications in 2018, Bentley and his colleagues found that the relationship between low income and high rates of obesity became noticeable on a national scale in the early 1990s. The 2018 study shows that the correlation between household income and obesity rate has grown steadily, from virtually no correlation in 1990 to a very strong correlation by 2016.
abstract •While many population health studies have invoked sugar as a major causal factor in the obesity epidemic, few have explicitly explored the temporal delay between increased sugar consumption and rising obesity rates.
•We model the increase of U.S. adult obesity since the 1990s as a legacy of increased consumption of excess sugars among children of the 1970s and 1980s.
•The model captures the generational time lag through a stochastic process of superfluous sugar calories increasing obesity rates over the lifespan of each birthyear cohort.
•Driven by annual USDA sugar consumption figures, the two-parameter model replicates three aspects of the data: Delayed timing and magnitude of the national rise in obesity since 1970.
•Profile of obesity rates by age group for a recent year.
•Change in obesity rates by age group among pre-adults.
•Our results indicate that past U.S. sugar consumption is at least sufficient to explain adult obesity change in the past 30 years.
In the last century, U.S. diets were transformed, including the addition of sugars to industrially-processed foods. While excess sugar has often been implicated in the dramatic increase in U.S. adult obesity over the past 30 years, an unexplained question is why the increase in obesity took place many years after the increases in U.S. sugar consumption. To address this, here we explain adult obesity increase as the cumulative effect of increased sugar calories consumed over time. In our model, which uses annual data on U.S. sugar consumption as the input variable, each age cohort inherits the obesity rate in the previous year plus a simple function of the mean excess sugar consumed in the current year. This simple model replicates three aspects of the data: (a) the delayed timing and magnitude of the increase in average U.S. adult obesity (from about 15% in 1970 to almost 40% by 2015); (b) the increase of obesity rates by age group (reaching 47% obesity by age 50) for the year 2015 in a well-documented U.S. state; and (c) the pre-adult increase of obesity rates by several percent from 1988 to the mid-2000s, and subsequent modest decline in obesity rates among younger children since the mid-2000s. Under this model, the sharp rise in adult obesity after 1990 reflects the delayed effects of added sugar calories consumed among children of the 1970s and 1980s.
how diabetes can increase cancer risk: dna damaged by high blood sugar
john termini et al. 2019
sciencedaily.com/releases/2019/08/190825075932.htm
Termini, who is at City of Hope, a research and treatment center for cancer and diabetes, had a different idea. He wondered if the elevated blood glucose levels seen in diabetes could harm DNA, making the genome unstable, which could lead to cancer. So Termini and colleagues looked for a specific type of damage in the form of chemically modified DNA bases, known as adducts, in tissue culture and rodent models of diabetes. Indeed, they found a DNA adduct, called N2-(1-carboxyethyl)-2'-deoxyguanosine, or CEdG, that occurred more frequently in the diabetic models than in normal cells or mice. What's more, high glucose levels interfered with the cells' process for fixing it. "Exposure to high glucose levels leads to both DNA adducts and the suppression of their repair, which in combination could cause genome instability and cancer," Termini says.
Recently, Termini and colleagues completed a clinical study that measured the levels of CEdG, as well as its counterpart in RNA (CEG), in people with type 2 diabetes. As in mice, people with diabetes had significantly higher levels of both CEdG and CEG than people without the disease.
But the team didn't stop there. They wanted to determine the molecular reasons why the adducts weren't being fixed properly by the cells. They identified two proteins that appear to be involved: the transcription factor HIF1α and the signaling protein mTORC1, which both show less activity in diabetes. HIF1α activates several genes involved in the repair process. "We found that if we stabilize HIF1α in a high-glucose environment, we increase DNA repair and reduce DNA damage," Termini says. "And mTORC1 actually controls HIF1α, so if you stimulate mTORC1, you stimulate HIF1α."
According to Termini, several drugs that stimulate HIF1α or mTORC1 already exist. The researchers plan to see if these drugs decrease cancer risk in diabetic animal models, and if so, they will test them in humans. Termini notes that metformin, a common diabetes medication that helps lower blood glucose levels, also stimulates DNA repair. "We're looking at testing metformin in combination with drugs that specifically stabilize HIF1α or enhance mTORC1 signaling in diabetic animal models," he says. In the meantime, a more immediate way for diabetics to reduce their cancer risk could be better control of their blood sugar. "That sounds like such an easy solution, but it's extremely difficult for most people to maintain glycemic control," Termini says.
short-term exposure to a western diet induces psoriasiform dermatitis by promoting accumulation of il-17a-producing γδ t cells
zhenrui shi et al. 2020
doi.org/10.1016/j.jid.2020.01.020
suggests that dietary components, rather than obesity itself, may lead to skin inflammation and the development of psoriasis. A common and chronic skin disease, psoriasis causes skin cells to form scales and red patches that are itchy and sometimes painful.
Diet and Skin Inflammation
Previous studies have shown that obesity is a risk factor for the development or worsening of psoriasis. The Western diet, characterized by a high dietary intake of saturated fats and sucrose and low intake of fiber, has been linked to the increased prevalence of obesity in the world.
“In our study, we found that short-term exposure to Western diet is able to induce psoriasis before significant body weight gain,” said Sam T. Hwang, professor and chair of dermatology at UC Davis and senior author on the study.
For the UC Davis Health study, which used a mouse model, Hwang and his colleagues found that a diet containing both high fat and high sugar (mimicking the Western diet in human) was required to induce observable skin inflammation. In four weeks only, mice on Western diet had significantly increased ear swelling and visible dermatitis compared to mice fed a controlled diet and those on high fat diet alone.
“Eating an unhealthy diet does not affect your waistline alone, but your skin immunity too,” said Zhenrui Shi, visiting assistant researcher in UC Davis Department of Dermatology and lead author on the study.
Bile Acids and Skin Inflammation
The study detailed the mechanisms by which inflammation happens following a Western diet. It identified bile acids as key signaling molecules in the regulation of skin immunity. Bile acids are produced in the liver from cholesterol and metabolized in the intestine by the gut microbiota. They play an important role in dietary lipid absorption and cholesterol balance in the blood.
The study found that cholestyramine, a drug used to lower cholesterol levels by binding to bile acids in the intestine, helped reduce the risk of skin inflammation. The finding suggests that bile acids mediate the development of psoriasis. The binding of cholestyramine to bile acids in the gut and its subsequent release through the stool allows for lowering of skin inflammation.
ten-hour time-restricted eating reduces weight, blood pressure, and atherogenic lipids in patients with metabolic syndrome
michael j. wilkinson et al. 2019
doi.org/10.1016/j.cmet.2019.11.004
“Eating and drinking everything (except water) within a consistent 10-hour window allows your body to rest and restore for 14 hours at night. Your body can also anticipate when you will eat so it can prepare to optimize metabolism,” says Emily Manoogian, the paper’s co-first author and a postdoctoral fellow in the Panda lab. “We wanted to know if controlling the timing of food intake to support circadian rhythms would improve the health of individuals that were already being treated for cardiometabolic diseases.”
The pilot study included 19 participants (13 men and 6 women) diagnosed with metabolic syndrome who self-reported eating during a time window of more than 14 hours per day. Additionally, 84 percent of participants were taking at least one medication such as a statin or an antihypertensive therapy. Study participants used the Panda lab’s myCircadianClock app to log when and what they ate during an initial 2-week baseline period followed by the three-month, 10-hour time-restricted eating intervention. Nearly 86 percent of participants correctly logged their food using the app, indicating high compliance throughout the study.
Participants did not report any adverse effects during the intervention. To reduce food intake to the 10-hour window, most participants delayed their first meal and advanced their last meal each day, so meals were not skipped. Although calories were not recommended to be reduced for the intervention, some participants did report eating less, likely due to the shorter eating window.
Overall, participants experienced improved sleep as well as a 3-4 percent reduction in body weight, body mass index, abdominal fat and waist circumference. Major risk factors for heart disease were diminished as participants showed reduced blood pressure and total cholesterol. Blood sugar levels and insulin levels also showed a trend toward improvement.
“Metabolism is closely linked with circadian rhythms, and knowing this, we were able to develop an intervention to help patients with metabolic syndrome without decreasing calories or increasing physical exercise,” says Pam Taub, co-corresponding author and associate professor of medicine at the UC San Diego School of Medicine and a cardiologist at UC San Diego Health. “If we can optimize circadian rhythms then we might be able to optimize the metabolic system.”
abstract •10 h time-restricted eating (TRE) in metabolic syndrome (MetS) promotes weight loss
•TRE in MetS reduces waist circumference, percent body fat, and visceral fat
•TRE in MetS lowers blood pressure, atherogenic lipids, and glycated hemoglobin
•Benefits of TRE are “add-ons” to statin and anti-hypertensive medications
In animal models, time-restricted feeding (TRF) can prevent and reverse aspects of metabolic diseases. Time-restricted eating (TRE) in human pilot studies reduces the risks of metabolic diseases in otherwise healthy individuals. However, patients with diagnosed metabolic syndrome often undergo pharmacotherapy, and it has never been tested whether TRE can act synergistically with pharmacotherapy in animal models or humans. In a single-arm, paired-sample trial, 19 participants with metabolic syndrome and a baseline mean daily eating window of ≥14 h, the majority of whom were on a statin and/or antihypertensive therapy, underwent 10 h of TRE (all dietary intake within a consistent self-selected 10 h window) for 12 weeks. We found this TRE intervention improves cardiometabolic health for patients with metabolic syndrome receiving standard medical care including high rates of statin and anti-hypertensive use. TRE is a potentially powerful lifestyle intervention that can be added to standard medical practice to treat metabolic syndrome.
opposing effects of fasting metabolism on tissue tolerance in bacterial and viral inflammation
andrew wang et al. 2020
doi.org/10.1016/j.cell.2016.07.026
abstract •Fasting metabolism is protective in bacterial, but not viral, inflammation
•Ketone bodies limit ROS-induced neuronal damage during bacterial inflammation
•Glucose utilization prevents UPR-mediated neuronal damage during viral inflammation
Acute infections are associated with a set of stereotypic behavioral responses, including anorexia, lethargy, and social withdrawal. Although these so-called sickness behaviors are the most common and familiar symptoms of infections, their roles in host defense are largely unknown. Here, we investigated the role of anorexia in models of bacterial and viral infections. We found that anorexia was protective while nutritional supplementation was detrimental in bacterial sepsis. Furthermore, glucose was necessary and sufficient for these effects. In contrast, nutritional supplementation protected against mortality from influenza infection and viral sepsis, whereas blocking glucose utilization was lethal. In both bacterial and viral models, these effects were largely independent of pathogen load and magnitude of inflammation. Instead, we identify opposing metabolic requirements tied to cellular stress adaptations critical for tolerance of differential inflammatory states.
fasting activates fatty acid oxidation to enhance intestinal stem cell function during homeostasis and aging
maria mihaylova et al. 2018
doi.org/10.1016/j.stem.2018.04.001
•Fasting induces fatty acid oxidation (FAO) in intestinal stem and progenitor cells
•Aging reduces ISC numbers and function, correlating with decreased FAO
•PPAR/CPT1a-mediated FAO augments ISC function in aging and during regeneration
•PPARδ agonists boost and restore ISC and progenitor function in young and old age
Diet has a profound effect on tissue regeneration in diverse organisms, and low caloric states such as intermittent fasting have beneficial effects on organismal health and age-associated loss of tissue function. The role of adult stem and progenitor cells in responding to short-term fasting and whether such responses improve regeneration are not well studied. Here we show that a 24 hr fast augments intestinal stem cell (ISC) function in young and aged mice by inducing a fatty acid oxidation (FAO) program and that pharmacological activation of this program mimics many effects of fasting. Acute genetic disruption of Cpt1a, the rate-limiting enzyme in FAO, abrogates ISC-enhancing effects of fasting, but long-term Cpt1a deletion decreases ISC numbers and function, implicating a role for FAO in ISC maintenance. These findings highlight a role for FAO in mediating pro-regenerative effects of fasting in intestinal biology, and they may represent a viable strategy for enhancing intestinal regeneration.
higher whole-grain intake is associated with lower risk of type 2 diabetes among middle-aged men and women: the danish diet, cancer, and health cohort
cecilie kyrø et al. 2018
doi.org/10.1093/jn/nxy112
The ability to use wholegrains for prevention of type 2 diabetes — previously sometimes known as adult-onset diabetes — has been known for a long time. But the role of different wholegrain sources has not been investigated. It has also been unclear how much wholegrain is needed to reduce the risk of developing diabetes.
“Most studies similar to ours have previously been conducted in the USA, where people mainly get their wholegrain from wheat,” says Rikard Landberg, Professor in Food and Health at Chalmers University of Technology, and senior researcher on the study. “We wanted to see if there was a difference between different cereals. One might expect there would be, because they contain different types of dietary fibre and bioactive substances, which have been shown to influence risk factors for type 2 diabetes.”
The study was conducted in Denmark, where there is a big variation in wholegrain-intake. The study showed that it made no difference which type of wholegrain product or cereal the participants ate — ryebread, oatmeal, and muesli, for example, seem to offer the same protection against type 2 diabetes.
What is more important is how much wholegrain one eats each day — and the study also provides important clarification to the scientific knowledge when it comes to daily dosages.
The participants were divided into 4 different groups, based on how much wholegrain they reported eating. Those with the highest consumption ate at least 50 grams of wholegrain each day. This corresponds to a portion of oatmeal porridge, and one slice of rye bread, for example.
The proportion who developed type 2 diabetes was lowest in the group which reported the highest wholegrain consumption, and increased for each group which had eaten less wholegrain. In the group with the highest wholegrain intake, the diabetes risk was 34 percent lower for men, and 22 percent lower for women, than in the group with the lowest wholegrain intake.
“It is unusual to be able to investigate such a large range when it comes to how much wholegrain people eat,” says Rikard Landberg. “If you divided American participants into 4 groups, the group that ate the most wholegrain would be the same level as the group that ate the least wholegrain in Denmark. In Europe, Scandinavia eats the most, Spain and Italy the least.”
Additionally, the study was uncommonly large, with 55,000 participants, over a long time span — 15 years.
If you compare wholegrains’ role in the risk of developing type 2 diabetes against other foods that have been investigated in other studies, it is one of the most effective ways to reduce the risk when it comes to diet. Drinking coffee, and avoiding red meat, are other factors that can similarly reduce the risk of type 2 diabetes.
“Our results are in line with dietary advice, which recommends switching out foods containing white flour for wholegrains,” says Rikard Landberg. “You get extra health benefits — white flour has some negative effects on health, while wholegrain has several positive effects, beyond protection against type 2 diabetes.”
Wholegrains are defined as consisting of all three main components of the grain kernel: endosperm, germ, and bran. Those who avoid all cereals, in an attempt to follow a low carb diet, therefore lose out on the positive health effects of wholegrain, which come principally from the bran and the germ. Rikard Landberg thinks that cereals, and carbohydrates in general, should not be avoided in diet.
“Carbohydrates are a very varied group of foodstuffs, including sugar, starch, and fibre. We should discuss these more individually, and not throw them together in one group, because they have totally different effects on our physiology and health. When it comes to wholegrains, the research results are clear: among the many studies which have been made, in varied groups of people around the world, there hasn’t been a single study which has shown negative health effects.”
abstract Whole-grain intake was associated with an 11% and 7% lower risk of type 2 diabetes per whole-grain serving (16 g) per day for men and women, respectively [HR (95% CI)—men: 0.89 (0.87, 0.91); women: 0.93 (0.91, 0.96)]. For men, the intake of all whole-grain cereal types investigated (wheat, rye, oats) was significantly associated with a lower risk of type 2 diabetes, but only wheat and oats intake was significantly associated for women. Among the different whole-grain products, rye bread, whole-grain bread, and oatmeal/muesli were significantly associated with a lower risk of type 2 diabetes for both men and women.
Conclusions
In this cohort study, we found consistent associations between high whole-grain intake and lower risk of type 2 diabetes. Overall, an association was found for all different cereals and whole-grain products tested.
adipose lipid turnover and long-term changes in body weight
p. arner et al. 2019
doi.org/10.1038/s41591-019-0565-5
studied the fat cells in 54 men and women over an average period of 13 years. In that time, all subjects, regardless of whether they gained or lost weight, showed decreases in lipid turnover in the fat tissue, that is the rate at which lipid (or fat) in the fat cells is removed and stored. Those who didn't compensate for that by eating less calories gained weight by an average of 20 percent, according to the study which was done in collaboration with researchers at Uppsala University in Sweden and University of Lyon in France.
The researchers also examined lipid turnover in 41 women who underwent bariatric surgery and how the lipid turnover rate affected their ability to keep the weight off four to seven years after surgery. The result showed that only those who had a low rate before the surgery managed to increase their lipid turnover and maintain their weight loss. The researchers believe these people may have had more room to increase their lipid turnover than those who already had a high-level pre-surgery.
"The results indicate for the first time that processes in our fat tissue regulate changes in body weight during ageing in a way that is independent of other factors," says Peter Arner, professor at the Department of Medicine in Huddinge at Karolinska Institutet and one of the study's main authors. "This could open up new ways to treat obesity."
Prior studies have shown that one way to speed up the lipid turnover in the fat tissue is to exercise more. This new research supports that notion and further indicates that the long-term result of weight-loss surgery would improve if combined with increased physical activity.
abstract The worldwide obesity epidemic1 makes it important to understand how lipid turnover (the capacity to store and remove lipids) regulates adipose tissue mass. Cross-sectional studies have shown that excess body fat is associated with decreased adipose lipid removal rates2,3. Whether lipid turnover is constant over the life span or changes during long-term weight increase or loss is unknown. We determined the turnover of fat cell lipids in adults followed for up to 16 years, by measuring the incorporation of nuclear bomb test-derived 14C in adipose tissue triglycerides. Lipid removal rate decreases during aging, with a failure to reciprocally adjust the rate of lipid uptake resulting in weight gain. Substantial weight loss is not driven by changes in lipid removal but by the rate of lipid uptake in adipose tissue. Furthermore, individuals with a low baseline lipid removal rate are more likely to remain weight-stable after weight loss. Therefore, lipid turnover adaptation might be important for maintaining pronounced weight loss. Together these findings identify adipose lipid turnover as an important factor for the long-term development of overweight/obesity and weight loss maintenance in humans.
twice as high diet-induced thermogenesis after breakfast vs dinner on high-calorie as well as low-calorie meals
kerstin m oltmanns et al. 2020
doi.org/10.1210/clinem/dgz311
Our body expends energy when we digest food for the absorption, digestion, transport and storage of nutrients. This process, known as diet-induced thermogenesis (DIT), is a measure of how well our metabolism is working, and can differ depending on mealtime.
“Our results show that a meal eaten for breakfast, regardless of the amount of calories it contains, creates twice as high diet-induced thermogenesis as the same meal consumed for dinner,” said the study’s corresponding author, Juliane Richter, M.Sc., Ph.D., of University of Lübeck in Germany. “This finding is significant for all people as it underlines the value of eating enough at breakfast.”
The researchers conducted a three-day laboratory study of 16 men who consumed a low-calorie breakfast and high-calorie dinner, and vice versa in a second round. They found identical calorie consumption led to 2.5 times higher DIT in the morning than in the evening after high-calorie and low-calorie meals. The food-induced increase of blood sugar and insulin concentrations was diminished after breakfast compared with dinner. The results also show eating a low-calorie breakfast increased appetite, specifically for sweets.
“We recommend that patients with obesity as well as healthy people eat a large breakfast rather than a large dinner to reduce body weight and prevent metabolic diseases,” Richter said.
abstract The question of whether there is daytime time variation in diet-induced thermogenesis (DIT) has not been clearly answered. Moreover, it is unclear whether a potential diurnal variation in DIT is preserved during hypocaloric nutrition.
Objective
We hypothesized that DIT varies depending on the time of day and explored whether this physiological regulation is preserved after low-calorie compared with high-calorie intake.
Design
Under blinded conditions, 16 normal-weight men twice underwent a 3-day in-laboratory, randomized, crossover study. Volunteers consumed a predetermined low-calorie breakfast (11% of individual daily kilocalorie requirement) and high-calorie dinner (69%) in one condition and vice versa in the other. DIT was measured by indirect calorimetry, parameters of glucose metabolism were determined, and hunger and appetite for sweets were rated on a scale.
Results
Identical calorie consumption led to a 2.5-times higher DIT increase in the morning than in the evening after high-calorie and low-calorie meals (P < .001). The food-induced increase of blood glucose and insulin concentrations was diminished after breakfast compared with dinner (P < .001). Low-calorie breakfast increased feelings of hunger (P < .001), specifically appetite for sweets (P = .007), in the course of the day.
Conclusions
DIT is clearly higher in the morning than in the evening, irrespective of the consumed calorie amount; that is, this physiological rhythmicity is preserved during hypocaloric nutrition. Extensive breakfasting should therefore be preferred over large dinner meals to prevent obesity and high blood glucose peaks even under conditions of a hypocaloric diet.
lipid droplet-derived monounsaturated fatty acids traffic via plin5 to allosterically activate sirt1
charles p. najt et al. 2020
http://dx.doi.org/10.1016/j.molcel.2019.12.003
Early studies on the diet suggested red wine was a major contributor to the health benefits of the Mediterranean diet because it contains a compound called resveratrol, which activated a certain pathway in cells known to increase lifespan and prevent aging-related diseases. However, work in Mashek’s lab suggests that it is the fat in olive oil, another component of the Mediterranean diet, that is actually activating this pathway.
According to Mashek, merely consuming olive oil is not enough to elicit all of the health benefits. His team’s studies suggest that when coupled with fasting, limiting caloric intake and exercising, the effects of consuming olive oil will be most pronounced.
“We found that the way this fat works is it first has to get stored in microscopic things called lipid droplets, which is how our cells store fat. And then, when the fat is broken down during exercising or fasting, for example, is when the signaling and beneficial effects are realized,” Mashek said.
abstract •MUFAs allosterically activate SIRT1 toward select substrates such as PGC-1α
•MUFAs enhance PGC-1α signaling in vivo in a SIRT1-dependent manner
•PLIN5 is a fatty acid binding protein that preferentially binds LD-derived MUFAs
•PLIN5 mediates MUFA signaling to control SIRT1/PGC-1α
Lipid droplets (LDs) provide a reservoir for triacylglycerol storage and are a central hub for fatty acid trafficking and signaling in cells. Lipolysis promotes mitochondrial biogenesis and oxidative metabolism via a SIRT1/PGC-1α/PPARα-dependent pathway through an unknown mechanism. Herein, we identify that monounsaturated fatty acids (MUFAs) allosterically activate SIRT1 toward select peptide-substrates such as PGC-1α. MUFAs enhance PGC-1α/PPARα signaling and promote oxidative metabolism in cells and animal models in a SIRT1-dependent manner. Moreover, we characterize the LD protein perilipin 5 (PLIN5), which is known to enhance mitochondrial biogenesis and function, to be a fatty-acid-binding protein that preferentially binds LD-derived monounsaturated fatty acids and traffics them to the nucleus following cAMP/PKA-mediated lipolytic stimulation. Thus, these studies identify the first-known endogenous allosteric modulators of SIRT1 and characterize a LD-nuclear signaling axis that underlies the known metabolic benefits of MUFAs and PLIN5.
eating breakfast and avoiding late-evening snacking sustains lipid oxidation
kevin parsons kelly et al. 2020
http://dx.doi.org/10.1371/journal.pbio.3000622
Your daily biological clock and sleep regulate how the food you eat is metabolized; thus the choice of burning fats or carbohydrates changes depending on the time of day or night. Your body’s circadian rhythm has programmed your body to burn fat when you sleep, so when you skip breakfast and then snack at night you delay burning the fat.
The researchers monitored the metabolism of mid-aged and older subjects in a whole-room respiratory chamber over two separate 56-hour sessions, using a “random crossover” experimental design. In each session, lunch and dinner were presented at the same times (12:30 and 17:45, respectively), but the timing of the third meal differed between the two halves of the study. Thus in one of the 56-hour bouts, the additional daily meal was presented as breakfast (8:00) whereas in the other session, a nutritionally equivalent meal was presented to the same subjects as a late-evening snack (22:00). The duration of the overnight fast was the same for both sessions.
Whereas the two sessions did not differ in the amount or type of food eaten or in the subjects’ activity levels, the daily timing of nutrient availability, coupled with clock/sleep control of metabolism, flipped a switch in the subjects’ fat/carbohydrate preference such that the late-evening snack session resulted in less fat burned when compared to the breakfast session. The timing of meals during the day/night cycle therefore affects the extent to which ingested food is used versus stored.
abstract Circadian (daily) regulation of metabolic pathways implies that food may be metabolized differentially over the daily cycle. To test that hypothesis, we monitored the metabolism of older subjects in a whole-room respiratory chamber over two separate 56-h sessions in a random crossover design. In one session, one of the 3 daily meals was presented as breakfast, whereas in the other session, a nutritionally equivalent meal was presented as a late-evening snack. The duration of the overnight fast was the same for both sessions. Whereas the two sessions did not differ in overall energy expenditure, the respiratory exchange ratio (RER) was different during sleep between the two sessions. Unexpectedly, this difference in RER due to daily meal timing was not due to daily differences in physical activity, sleep disruption, or core body temperature (CBT). Rather, we found that the daily timing of nutrient availability coupled with daily/circadian control of metabolism drives a switch in substrate preference such that the late-evening Snack Session resulted in significantly lower lipid oxidation (LO) compared to the Breakfast Session. Therefore, the timing of meals during the day/night cycle affects how ingested food is oxidized or stored in humans, with important implications for optimal eating habits.
afternoon distraction: a high-saturated-fat meal and endotoxemia impact postmeal attention in a randomized crossover trial
janice k kiecolt-glaser et al. 2020
http://dx.doi.org/10.1093/ajcn/nqaa085
compared how 51 women performed on a test of their attention after they ate either a meal high in saturated fat or the same meal made with sunflower oil, which is high in unsaturated fat.
Their performance on the test was worse after eating the high-saturated-fat meal than after they ate the meal containing a healthier fat, signaling a link between that fatty food and the brain.
Researchers were also looking at whether a condition called leaky gut, which allows intestinal bacteria to enter the bloodstream, had any effect on concentration. Participants with leakier guts performed worse on the attention assessment no matter which meal they had eaten.
The loss of focus after a single meal was eye-opening for the researchers.
“Most prior work looking at the causative effect of the diet has looked over a period of time. And this was just one meal — it’s pretty remarkable that we saw a difference,” said Annelise Madison, lead author of the study and a graduate student in clinical psychology at The Ohio State University.
Madison also noted that the meal made with sunflower oil, while low in saturated fat, still contained a lot of dietary fat.
“Because both meals were high-fat and potentially problematic, the high-saturated-fat meal’s cognitive effect could be even greater if it were compared to a lower-fat meal,” she said.
The study is published in the American Journal of Clinical Nutrition.
Madison works in the lab of Janice Kiecolt-Glaser, professor of psychiatry and psychology and director of the Institute for Behavioral Medicine Research at Ohio State. For this work, Madison conducted a secondary analysis of data from Kiecolt-Glaser’s study assessing whether high-fat meals increased fatigue and inflammation among cancer survivors.
Women in the study completed a baseline assessment of their attention during a morning visit to the lab. The tool, called a continuous performance test, is a measure of sustained attention, concentration and reaction time based on 10 minutes of computer-based activities.
The high-fat meal followed: eggs, biscuits, turkey sausage and gravy containing 60 grams of fat, either a palmitic acid-based oil high in saturated fat or the lower-saturated-fat sunflower oil. Both meals totaled 930 calories and were designed to mimic the contents of various fast-food meals such as a Burger King double whopper with cheese or a McDonald’s Big Mac and medium fries.
Five hours later, the women took the continuous performance test again. Between one and four weeks later, they repeated these steps, eating the opposite meal of what they had eaten on the first visit.
Researchers also analyzed participants’ fasting baseline blood samples to determine whether they contained an inflammatory molecule that signals the presence of endotoxemia — the toxin that escapes from the intestines and enters the bloodstream when the gut barrier is compromised.
After eating the meal high in saturated fat, all of the participating women were, on average, 11 percent less able to detect target stimuli in the attention assessment. Concentration lapses were also apparent in the women with signs of leaky gut: Their response times were more erratic and they were less able to sustain their attention during the 10-minute test.
“If the women had high levels of endotoxemia, it also wiped out the between-meal differences. They were performing poorly no matter what type of fat they ate,” Madison said.
Though the study didn’t determine what was going on in the brain, Madison said previous research has suggested that food high in saturated fat can drive up inflammation throughout the body, and possibly the brain. Fatty acids also can cross the blood-brain barrier.
“It could be that fatty acids are interacting with the brain directly. What it does show is the power of gut-related dysregulation,” she said.
The statistical analysis accounted for other potential influences on cognition, including depressive symptoms and the participants’ average dietary saturated fat consumption. The women in the study ate three standardized meals and fasted for 12 hours before each lab visit to reduce diet variations that could affect their physiological response to the high-fat meals.
The findings suggest concentration could be even more impaired in people stressed by the pandemic who are turning to fatty foods for comfort, Kiecolt-Glaser said.
“What we know is that when people are more anxious, a good subset of us will find high-saturated-fat food more enticing than broccoli,” she said. “We know from other research that depression and anxiety can interfere with concentration and attention as well. When we add that on top of the high-fat meal, we could expect the real-world effects to be even larger.”
abstract Background
Saturated-fat intake and endotoxemia can impair cognition. However, their acute impact on cognitive performance is unknown.
Objective
This study assessed the impact of 2 high-fat meals and endotoxemia on attention.
Methods
In this double-blind, randomized crossover trial, 51 women (n = 32 breast cancer survivors, n = 19 noncancer controls; mean ± SD age: 53 ± 8 y) completed the Continuous Performance Test (CPT) and had their blood drawn to assess endotoxemia markers LPS binding protein (LBP), soluble CD14 (sCD14), and the LBP to sCD14 ratio 1 h prior to eating either a high-saturated-fat meal or a high-oleic-sunflower-oil meal. Women again completed the CPT 5 h postmeal. At 1 to 4 wk later, women completed the same protocol but consumed the other meal.
Results
In adjusted models, women had more difficulty distinguishing target stimuli from distractors after consuming the high-saturated-fat meal than they did after the oleic-sunflower-oil meal (B = 4.44, SE = 1.88, P = 0.02). Women with higher baseline LBP had less consistent response times (B = 0.002, SE = 0.0008, P = 0.04). Those with higher LBP and LBP:sCD14 were less able to sustain their attention throughout the entire CPT, as reflected by their progressively slower (B = 0.002, SE = 0.0006, P = 0.003; and B = 2.43, SE = 0.090, P = 0.008, respectively) and more erratic (B = 0.003, SE = 0.0008, P < 0.0001; and B = 3.29, SE = 1.17, P = 0.006, respectively) response times. Additionally, women with higher baseline LBP or sCD14 were less able to maintain or increase response speeds at higher interstimulus intervals (B = 0.002, SE = 0.0006, P = 0.02; and B = 0.006, SE = 0.003, P = 0.03, respectively), indicating greater difficulty adapting to changing task demands. Significant meal type by LBP and LBP:sCD14 interactions emerged (P < 0.05), such that high LBP and LBP:sCD14 erased between-meal cognitive differences, uniformly impairing performance.
Conclusions
These results suggest that higher LBP, sCD14, and LBP:sCD14 and saturated-fat intake individually and jointly influence attention. Endotoxemia may override the relative cognitive benefit of healthier oil choices.
obesity shapes metabolism in the tumor microenvironment to suppress anti-tumor immunity
alison e. ringel et al. 2020
doi.org/10.1016/j.cell.2020.11.009
a high-fat diet reduces the numbers and antitumor activity of CD8+ T cells, a critical type of immune cell, inside tumors. This occurs because cancer cells reprogram their metabolism in response to increased fat availability to better gobble up energy-rich fat molecules, depriving T cells of fuel and accelerating tumor growth.
"Putting the same tumor in obese and nonobese settings reveals that cancer cells rewire their metabolism in response to a high fat diet," said Marcia Haigis, professor of cell biology in the Blavatnik Institute at HMS and co-senior author of the study. "This finding suggests that a therapy that would potentially work in one setting might not be as effective in another, which needs to be better understood given the obesity epidemic in our society."
The team found that blocking this fat-related metabolic reprogramming significantly reduced tumor volume in mice on high-fat diets. Because CD8+ T cells are the main weapon used by immunotherapies that activate the immune system against cancer, the study results suggest new strategies for improving such therapies.
"Cancer immunotherapies are making an enormous impact on patients' lives, but they do not benefit everyone," said co-senior author Arlene Sharpe, the HMS George Fabyan Professor of Comparative Pathology and chair of the Department of Immunology in the Blavatnik Institute.
"We now know there is a metabolic tug-of-war between T cells and tumor cells that changes with obesity," Sharpe said. "Our study provides a roadmap to explore this interplay, which can help us to start thinking about cancer immunotherapies and combination therapies in new ways."
Haigis, Sharpe and colleagues investigated the effects of obesity on mouse models of different types of cancer, including colorectal, breast, melanoma and lung. Led by study co-first authors Alison Ringel and Jefte Drijvers, the team gave mice normal or high-fat diets, the latter leading to increased body weight and other obesity-related changes. They then looked at different cell types and molecules inside and around tumors, together called the tumor microenvironment.
Fatty paradox
The researchers found that tumors grew much more rapidly in animals on high-fat diets compared to those on normal diets. But this occurred only in cancer types that are immunogenic, which can contain high numbers of immune cells; are more easily recognized by the immune system; and are more likely to provoke an immune response.
Experiments revealed that diet-related differences in tumor growth depended specifically on the activity of CD8+ T cells, immune cells that can target and kill cancer cells. Diet did not affect tumor growth rate if CD8+ T cells were eliminated experimentally in mice.
Strikingly, high-fat diets reduced the presence of CD8+ T cells in the tumor microenvironment, but not elsewhere in the body. Those remaining in the tumor were less robust -- they divided more slowly and had markers of decreased activity. But when these cells were isolated and grown in a lab, they had normal activity, suggesting something in the tumor impaired these cells' function.
The team also encountered an apparent paradox. In obese animals, the tumor microenvironment was depleted of key free fatty acids, a major cellular fuel source, even though the rest of the body was enriched in fats, as expected in obesity.
These clues pushed the researchers to craft a comprehensive atlas of the metabolic profiles of different cell types in tumors under normal and high-fat diet conditions.
The analyses revealed that cancer cells adapted in response to changes in fat availability. Under a high-fat diet, cancer cells were able to reprogram their metabolism to increase fat uptake and utilization, while CD8+ T cells did not. This ultimately depleted the tumor microenvironment of certain fatty acids, leaving T cells starved for this essential fuel.
"The paradoxical depletion of fatty acids was one of the most surprising findings of this study. It really blew us away and it was the launch pad for our analyses," said Ringel, a postdoctoral fellow in the Haigis lab. "That obesity and whole-body metabolism can change how different cells in tumors utilize fuel was an exciting discovery, and our metabolic atlas now allows us to dissect and better understand these processes."
Hot and cold
Through several different approaches, including single-cell gene expression analyses, large-scale protein surveys and high-resolution imaging, the team identified numerous diet-related changes to metabolic pathways of both cancer and immune cells in the tumor microenvironment.
Of particular interest was PHD3, a protein that in normal cells has been shown to act as a brake on excessive fat metabolism. Cancer cells in an obese environment had significantly lower expression of PHD3 compared to in a normal environment. When the researchers forced tumor cells to overexpress PHD, they found that this diminished a tumor's ability to take up fat in obese mice. It also restored the availability of key free fatty acids in the tumor microenvironment.
Increased PHD3 expression largely reversed the negative effects of a high-fat diet on immune cell function in tumors. Tumors with high PHD3 grew slower in obese mice compared to tumors with low PHD3. This was a direct result of increased CD8+ T cell activity. In obese mice lacking CD8+ T cells, tumor growth was unaffected by differences in PHD3 expression.
The team also analyzed human tumor databases and found that low PHD3 expression was associated with immunologically "cold" tumors, defined by fewer numbers of immune cells. This association suggested that tumor fat metabolism plays a role in human disease, and that obesity reduces antitumor immunity in multiple cancer types, the authors said.
"CD8+ T cells are the central focus of many promising precision cancer therapies, including vaccines and cell therapies such as CAR-T," Sharpe said. "These approaches need T cells to have sufficient energy to kill cancer cells, but at the same time we don't want tumors to have fuel to grow. We now have amazingly comprehensive data for studying this dynamic and determining mechanisms that prevent T cells from functioning as they should."
abstract demonstrate that high-fat diet (HFD)-induced obesity impairs CD8 + T cell function in the murine TME, accelerating tumor growth. We generate a single-cell resolution atlas of cellular metabolism in the TME, detailing how it changes with diet-induced obesity. We find that tumor and CD8 + T cells display distinct metabolic adaptations to obesity. Tumor cells increase fat uptake with HFD, whereas tumor-infiltrating CD8 + T cells do not. These differential adaptations lead to altered fatty acid partitioning in HFD tumors, impairing CD8 + T cell infiltration and function.
early micronutrient supplementation protects against early stress-induced cognitive impairments
e. f. g. naninck et al. 2016
intestinal dysmotility syndromes following systemic infection by flaviviruses
james p. white et al. 2018
http://dx.doi.org/10.1016/j.cell.2018.08.069
•Infection with multiple flaviviruses causes delayed gastrointestinal transit
•Dysmotility and neuronal death are caused by infiltrating antiviral CD8 + T cells
•Surviving animals exhibit long-term chronic gastrointestinal dysmotility
•Chronic dysmotility is exacerbated by exposure to unrelated inflammatory stimuli
Although chronic gastrointestinal dysmotility syndromes are a common worldwide health problem, underlying causes for these disorders are poorly understood. We show that flavivirus infection of enteric neurons leads to acute neuronal injury and cell death, inflammation, bowel dilation, and slowing of intestinal transit in mice. Flavivirus-primed CD8 + T cells promote these phenotypes, as their absence diminished enteric neuron injury and intestinal transit delays, and their adoptive transfer reestablished dysmotility after flavivirus infection. Remarkably, mice surviving acute flavivirus infection developed chronic gastrointestinal dysmotility that was exacerbated by immunization with an unrelated alphavirus vaccine or exposure to a non-infectious inflammatory stimulus. This model of chronic post-infectious gastrointestinal dysmotility in mice suggests that viral infections with tropism for enteric neurons and the ensuing immune response might contribute to the development of bowel motility disorders in humans. These results suggest an opportunity for unique approaches to diagnosis and therapy of gastrointestinal dysmotility syndromes.
food color is in the eye of the beholder: the role of human trichromatic vision in food evaluation
francesco foroni, giulio pergola, raffaella ida rumiati 2016
srep37034
neanderthals in cold regions probably ate a lot more vegetable food than was previously thought, according to new research on ancient neanderthal dental plaque.
coastal groundwater discharge and the ancient inhabitants of rapa nui (easter island), chile
tanya brosnan et al. 2018
http://dx.doi.org/10.1007/s10040-018-1870-7
development of gluten-free rice bread: pickering stabilization as a possible batter-swelling mechanism
hiroyuki yano, akiko fukui, keiko kajiwara, isao kobayashi, koh-ichi yoza, akiyoshi satake, masumi villeneuve 2017
dx.doi.org/10.1016/j.lwt.2016.11.086
kenny mediates selective autophagic degradation of the ikk complex to control innate immune responses
radu tusco et al. 2017
dx.doi.org/10.1038/s41467-017-01287-9
methionine metabolism shapes t helper cell responses through regulation of epigenetic reprogramming
dominic g. roy et al. 2020
http://dx.doi.org/10.1016/j.cmet.2020.01.006
While many cell types in the body produce methionine, the immune cells responsible for responding to threats like pathogens do not. Instead, the methionine that fuels these specialized cells, called T cells, must be ingested through food consumption. Although methionine is found in most foods, animal products such as meat and eggs contain particularly high levels.
“Methionine is critical for a healthy immune system. Our results suggest, for people predisposed to inflammatory and autoimmune disorders like multiple sclerosis, reducing methionine intake can actually dampen the immune cells that cause disease, leading to better outcomes” said Russell Jones, Ph.D., the study’s senior author and program leader of Van Andel Institute’s Metabolic and Nutritional Programming group. “These findings provide further basis for dietary interventions as future treatments for these disorders.”
Autoimmune disorders occur when the immune system mistakenly attacks and destroys healthy tissue. For example, in multiple sclerosis — the most common inflammatory disease of the central nervous system — the myelin sheath that protects nerve cells in the brain and spinal cord is targeted by the immune system. The subsequent damage impedes messages traveling to and from the brain, resulting in progressively worsening symptoms like numbness, muscle weakness, coordination and balance problems, and cognitive decline. There currently are no treatments that significantly slow or stop multiple sclerosis without greatly increasing the risk of infection or cancer.
“What causes multiple sclerosis is still not completely understood. We know that genes related to the immune system are implicated but environmental factors also have a role to play,” said Catherine Larochelle, M.D., Ph.D., study co-author, and a clinician-scientist in neuroimmunology and neurologist at the Multiple Sclerosis Clinic at the Centre Hospitalier de l’Université de Montréal. “The fact that metabolic factors like obesity increase the risk of developing multiple sclerosis makes the idea of dietary intervention to calm down the immune system particularly appealing.”
During an immune response, T cells flood the affected area to help the body fend off pathogens. Jones, Larochelle and their teams found dietary methionine fuels this process by helping “reprogram” T cells to respond to the threat by more quickly replicating and differentiating into specialized subtypes. Some of these reprogrammed T cells cause inflammation, which is a normal part of an immune response but can cause damage if it lingers, such as the nerve damage that occurs in multiple sclerosis.
The researchers also found that significantly reducing methionine in the diets of mouse models of multiple sclerosis altered the reprogramming of T cells, limiting their ability to cause inflammation in the brain and spinal cord. The result was a delay in the disease’s onset and slowed progression.
“By restricting methionine in the diet, you’re essentially removing the fuel for this over-active inflammatory response without compromising the rest of the immune system,” Jones said.
abstract •Activated T cells use exogenous methionine to synthesize the methyl donor SAM
•Methionine restriction reduces intracellular SAM and H3K4me3 levels in T cells
•Methionine restriction limits the expansion of inflammatory Th17 cells
•EAE onset and severity are reduced by dietary methionine restriction
Epigenetic modifications on DNA and histones regulate gene expression by modulating chromatin accessibility to transcription machinery. Here we identify methionine as a key nutrient affecting epigenetic reprogramming in CD4 + T helper (Th) cells. Using metabolomics, we showed that methionine is rapidly taken up by activated T cells and serves as the major substrate for biosynthesis of the universal methyl donor S-adenosyl-L-methionine (SAM). Methionine was required to maintain intracellular SAM pools in T cells. Methionine restriction reduced histone H3K4 methylation (H3K4me3) at the promoter regions of key genes involved in Th17 cell proliferation and cytokine production. Applied to the mouse model of multiple sclerosis (experimental autoimmune encephalomyelitis), dietary methionine restriction reduced the expansion of pathogenic Th17 cells in vivo, leading to reduced T cell-mediated neuroinflammation and disease onset. Our data identify methionine as a key nutritional factor shaping Th cell proliferation and function in part through regulation of histone methylation.
deep pelagic food web structure as revealed by in situ feeding observations
c. anela choy et al. 2017
http://dx.doi.org/10.1098/rspb.2017.2116
the opportunity cost of animal based diets exceeds all food losses
alon shepon et al. 2018
http://dx.doi.org/10.1073/pnas.1713820115
charlotte payne
libertyruth.com/
edible insects and human evolution
julie j. lesnik 2018 unread
0813056993
the lion king
food intake recruits orosensory and post-ingestive dopaminergic circuits to affect eating desire in humans
sharmili edwin thanarajah et al. 2018
http://dx.doi.org/10.1016/j.cmet.2018.12.006
dopamine release in the brain occurs at two different times: at the time the food is first ingested and another once the food reaches the stomach. The work appears December 27 in the journal Cell Metabolism.
"With the help of a new positron emission tomography (PET) technique we developed, we were not only able to find the two peaks of dopamine release, but we could also identify the specific brain regions that were associated with these releases," says senior author Marc Tittgemeyer, head of the Institute's Translational Neurocircuitry Group. "While the first release occurred in brain regions associated with reward and sensory perception, the post-ingestive release involved additional regions related to higher cognitive functions."
In the study, 12 healthy volunteers received either a palatable milkshake or a tasteless solution while PET data were recorded. Interestingly, the subjects' craving or desire for the milkshake was proportionally linked to the amount of dopamine released in particular brain areas at the first tasting. But the higher the craving, the less delayed post-ingestive dopamine was released.
"On one hand, dopamine release mirrors our subjective desire to consume a food item. On the other hand, our desire seems to suppress gut-induced dopamine release," says Heiko Backes, group leader for Multimodal Imaging of Brain Metabolism at the Institute, who is co-first author on the study with Sharmili Edwin Thanarajah.
Suppression of gut-induced release could potentially cause overeating of highly desired food items. "We continue to eat until sufficient dopamine was released," Backes says but adds that this hypothesis remains to be tested in further studies.
Earlier experiments have demonstrated gut-induced dopamine release in mice, but this is the first time it has been shown in humans.
abstract •Food intake induces orosensory and post-ingestive dopamine release in humans
•Both recruit distinct pathways: orosensory integrative and higher cognitive centers
•Dopamine release in “wanting”-associated regions mirrors subjective desire to eat
•Post-ingestive dopamine release in the putamen is inversely correlated to “wanting”
Pleasant taste and nutritional value guide food selection behavior. Here, orosensory features of food may be secondary to its nutritional value in underlying reinforcement, but it is unclear how the brain encodes the reward value of food. Orosensory and peripheral physiological signals may act together on dopaminergic circuits to drive food intake. We combined fMRI and a novel [11C]raclopride PET method to assess systems-level activation and dopamine release in response to palatable food intake in humans. We identified immediate orosensory and delayed post-ingestive dopamine release. Both responses recruit segregated brain regions: specialized integrative pathways and higher cognitive centers. Furthermore, we identified brain areas where dopamine release reflected the subjective desire to eat. Immediate dopamine release in these wanting-related regions was inversely correlated with, and presumably inhibited, post-ingestive release in the dorsal striatum. Our results highlight the role of brain and periphery in interacting to reinforce food intake in humans.
central amygdala prepronociceptin-expressing neurons mediate palatable food consumption and reward
j. andrew hardaway et al. 2019
http://dx.doi.org/10.1016/j.neuron.2019.03.037
a specific network of cellular communication emanating from the emotion-processing region of the brain, motivating mice to keep eating tasty food even though their basic energy needs had been met.
The existence of this mammalian brain circuit, described in a paper in Neuron, might help explain why humans so often overeat in our modern environment of abundant and delicious fare. The circuit is a byproduct of evolution, when large calorie-rich meals were scarce, and so our brains were wired to devour as many calories as humanly possible because no one knew when the next super meal would come.
"This circuit seems to be the brain's way of telling you that if something tastes really good, then it's worth whatever price you're paying to get to it, so don't stop," Kash said.
Scientists in search of anti-obesity remedies have spent decades researching and targeting brain cells and circuits involved in ordinary, "homeostatic" feeding, which is triggered by hunger and keeps our energy level up. But this approach has had limited success. More recently, some scientists have been studying "hedonic" feeding -- the pleasure-driven eating of calorie-rich food that tends to go way beyond our strict energy needs.
Hedonic feeding is thought to reflect modern humans' lingering adaptation for ancient environments where famines were frequent. Perceiving calorie-rich food as particularly tasty and pleasurable, and bingeing on it whenever it was available, would have conferred a crucial survival advantage by storing up extra energy. Following that instinct now, in a time of plenty, can lead to obesity -- a condition affecting about 40 percent of adults in the United States -- and related conditions such as diabetes, heart disease, and cancers.
"There's just so much calorically dense food available all the time now, and we haven't yet lost this wiring that influences us to eat as much food as possible," Kash said.
Experiments in the past few years have suggested that our wiring for hedonic feeding involves nociceptin, a small protein that works as a signaling molecule in the mammalian nervous system. Kash's laboratory and other groups have found that compounds blocking nociceptin activity -- called nociceptin receptor antagonists -- have little or no effect on homeostatic feeding by lab rats and mice, but these compounds do curb hedonic bingeing on tasty, calorie-rich foods. Thus, drug developers have eyed these antagonists as potential anti-obesity, anti-binge-eating drugs, and researchers have been eager to identify the specific brain circuits through which they work. The goal would be to develop a more targeted treatment.
Identifying this circuit is largely what Kash and colleagues accomplished in their new study. They engineered mice to produce a fluorescent molecule along with nociceptin, literally illuminating the cells that drive nociceptin circuits. There are multiple nociceptin circuits in the brain, but Kash and colleagues observed that one in particular became active when the mice got a chance to binge on calorie-rich food. The circuit projects to different parts of the brain, including those known to regulate feeding. It starts in an emotion-processing region of the brain called the central amygdala.
Deleting about half of the nociceptin-making neurons in this circuit reduced the mice's bingeing and kept their weight down when they had access to rich food, without affecting their intake of ordinary chow.
"Scientists have studied the amygdala for a long time, and they've linked it to pain and anxiety and fear, but our findings here highlight that it does other things too, like regulate pathological eating," Kash said.
He and his team are now studying in more detail how this circuit works, the timing of its activity in relation to feeding and other factors, and how nociceptin antagonists alter its functions.
First author J. Andrew Hardaway, PhD, research assistant professor of pharmacology at the UNC School of Medicine, said, "Our study is one of the first to describe how the brain's emotional center contributes to eating for pleasure. It adds support to the idea that everything mammals eat is being dynamically categorized along a spectrum of good/tasty to bad/disgusting, and this may be physically represented in subsets of neurons in the amygdala. The next major step and challenge is to tap into these subsets to derive new therapeutics for obesity and binge eating."
Other scientists are studying nociceptin antagonists as possible treatments not only for obesity and binge-eating but also for depression, pain, and substance abuse.
"The behavioral effects of blocking nociceptin activity probably involve multiple mechanisms in the brain," Kash said. "But on the whole, blocking nociceptin seems to stabilize behavior, bringing it closer to normal."
abstract Food palatability is one of many factors that drives food consumption, and the hedonic drive to feed is a key contributor to obesity and binge eating. In this study, we identified a population of prepronociceptin-expressing cells in the central amygdala ( Pnoc CeA) that are activated by palatable food consumption. Ablation or chemogenetic inhibition of these cells reduces palatable food consumption. Additionally, ablation of Pnoc CeA cells reduces high-fat-diet-driven increases in bodyweight and adiposity. Pnoc CeA neurons project to the ventral bed nucleus of the stria terminalis (vBNST), parabrachial nucleus (PBN), and nucleus of the solitary tract (NTS), and activation of cell bodies in the central amygdala (CeA) or axons in the vBNST, PBN, and NTS produces reward behavior but did not promote feeding of palatable food. These data suggest that the Pnoc CeA network is necessary for promoting the reinforcing and rewarding properties of palatable food, but activation of this network itself is not sufficient to promote feeding.
litchi fruit contains methylene cyclopropyl-glycine
mukul das et al. 2015
http://www.currentscience.ac.in/volumes/109/12/2195.pdf
lychees
cross-sectional association of seafood consumption, polyunsaturated fatty acids and depressive symptoms in two torres strait communities
maximus berger et al. 2018
http://dx.doi.org/10.1080/1028415X.2018.1504429
hydraulic redistribution by native sahelian shrubs: bioirrigation to resist in-season drought
nathaniel a. bogie et al. 2018
http://dx.doi.org/10.3389/fenvs.2018.00098
the association between mushroom consumption and mild cognitive impairment: a community-based cross-sectional study in singapore
lei feng et al. 2019
http://dx.doi.org/10.3233/jad-180959
A portion was defined as three quarters of a cup of cooked mushrooms with an average weight of around 150 grams. Two portions would be equivalent to approximately half a plate. While the portion sizes act as a guideline, it was shown that even one small portion of mushrooms a week may still be beneficial to reduce chances of MCI.
"This correlation is surprising and encouraging. It seems that a commonly available single ingredient could have a dramatic effect on cognitive decline," said Assistant Professor Lei Feng, who is from the NUS Department of Psychological Medicine, and the lead author of this work.
The six-year study, which was conducted from 2011 to 2017, collected data from more than 600 Chinese seniors over the age of 60 living in Singapore. The research was carried out with support from the Life Sciences Institute and the Mind Science Centre at NUS, as well as the Singapore Ministry of Health's National Medical Research Council. The results were published online in the Journal of Alzheimer's Disease on 12 March 2019.
Determining MCI in seniors
MCI is typically viewed as the stage between the cognitive decline of normal ageing and the more serious decline of dementia. Seniors afflicted with MCI often display some form of memory loss or forgetfulness and may also show deficit on other cognitive function such as language, attention and visuospatial abilities. However, the changes can be subtle, as they do not experience disabling cognitive deficits that affect everyday life activities, which is characteristic of Alzheimer's and other forms of dementia.
"People with MCI are still able to carry out their normal daily activities. So, what we had to determine in this study is whether these seniors had poorer performance on standard neuropsychologist tests than other people of the same age and education background," explained Asst Prof Feng. "Neuropsychological tests are specifically designed tasks that can measure various aspects of a person's cognitive abilities. In fact, some of the tests we used in this study are adopted from commonly used IQ test battery, the Wechsler Adult Intelligence Scale (WAIS)."
As such, the researchers conducted extensive interviews and tests with the senior citizens to determine an accurate diagnosis. "The interview takes into account demographic information, medical history, psychological factors, and dietary habits. A nurse will measure blood pressure, weight, height, handgrip, and walking speed. They will also do a simple screen test on cognition, depression, anxiety," said Asst Prof Feng.
After this, a two-hour standard neuropsychological assessment was performed, along with a dementia rating. The overall results of these tests were discussed in depth with expert psychiatrists involved in the study to get a diagnostic consensus.
Mushrooms and cognitive impairment
Six commonly consumed mushrooms in Singapore were referenced in the study. They were golden, oyster, shiitake and white button mushrooms, as well as dried and canned mushrooms. However, it is likely that other mushrooms not referenced would also have beneficial effects.
The researchers believe the reason for the reduced prevalence of MCI in mushroom eaters may be down to a specific compound found in almost all varieties. "We're very interested in a compound called ergothioneine (ET)," said Dr Irwin Cheah, Senior Research Fellow at the NUS Department of Biochemistry. "ET is a unique antioxidant and anti-inflammatory which humans are unable to synthesise on their own. But it can be obtained from dietary sources, one of the main ones being mushrooms."
An earlier study by the team on elderly Singaporeans revealed that plasma levels of ET in participants with MCI were significantly lower than age-matched healthy individuals. The work, which was published in the journal Biochemical and Biophysical Research Communications in 2016, led to the belief that a deficiency in ET may be a risk factor for neurodegeneration, and increasing ET intake through mushroom consumption might possibly promote cognitive health.
Other compounds contained within mushrooms may also be advantageous for decreasing the risk of cognitive decline. Certain hericenones, erinacines, scabronines and dictyophorines may promote the synthesis of nerve growth factors. Bioactive compounds in mushrooms may also protect the brain from neurodegeneration by inhibiting production of beta amyloid and phosphorylated tau, and acetylcholinesterase.
Next steps
The potential next stage of research for the team is to perform a randomised controlled trial with the pure compound of ET and other plant-based ingredients, such as L-theanine and catechins from tea leaves, to determine the efficacy of such phytonutrients in delaying cognitive decline. Such interventional studies will lead to more robust conclusion on causal relationship. In addition, Asst Prof Feng and his team also hope to identify other dietary factors that could be associated with healthy brain ageing and reduced risk of age-related conditions in the future.
abstract We examined the cross-sectional association between mushroom intake and mild cognitive impairment (MCI) using data from 663 participants aged 60 and above from the Diet and Healthy Aging (DaHA) study in Singapore. Compared with participants who consumed mushrooms less than once per week, participants who consumed mushrooms >2 portions per week had reduced odds of having MCI (odds ratio = 0.43, 95% CI 0.23–0.78, p = 0.006) and this association was independent of age, gender, education, cigarette smoking, alcohol consumption, hypertension, diabetes, heart disease, stroke, physical activities, and social activities. Our cross-sectional data support the potential role of mushrooms and their bioactive compounds in delaying neurodegeneration.
interplay between mitochondria and diet mediates pathogen and stress resistance in caenorhabditis elegans
alexey v. revtovich et al. 2019
http://dx.doi.org/10.1371/journal.pgen.1008011
Despite their simplicity, 1-millimeter-long nematodes called Caenorhabditis elegans (C. elegans) share an important limitation with humans: They cannot make B12 and must get all they need from their diet. In a study published today in PLOS Genetics, researchers from the lab of Rice biochemist and cancer researcher Natasha Kirienko describe how a B12-deficient diet harms C. elegans' health at a cellular level, reducing the worms' ability to metabolize branched-chain amino acids (BCAA). The research showed that the reduced ability to break down BCAAs led to a toxic buildup of partially metabolized BCAA byproducts that damaged mitochondrial health.
Researchers studied the health of two populations of worms, one with a diet sufficient in B12 and another that got too little B12 from its diet. Like the second population of worms, at least 10 percent of U.S. adults get too little B12 in their diet, a risk that increases with age.
"We used C. elegans to study the effect of diet on a host and found that one kind of food was able to dramatically increase resistance to multiple stressors -- like heat and free radicals -- as well as to pathogens," said Kirienko, assistant professor of biosciences and a CPRIT Scholar in Cancer Research at Rice.
The lead scientist and co-author of the study, Kirienko said the B12 finding came as a surprise to her team, which first noticed the effect in experiments designed to investigate the mechanisms of pathogenesis of Pseudomonas aeruginosa (P. aeruginosa), a potentially deadly disease in both worms and humans that infects some 51,000 U.S. hospital patients each year, according to the Centers for Disease Control.
Her lab, like thousands of others worldwide, uses C. elegans as a model organism to study the effects of disease, drugs, toxins and other processes that affect humans and animals. In many C. elegans research labs worms are fed Escherichia coli (E. coli), a common human gut bacteria that is itself a model organism.
"We found that switching between E. coli strain OP50 and strain HT115 dramatically altered the worm's stress tolerance," Kirienko said. She said it took about two years of follow-up studies to isolate the biochemical mechanism of stress and pathogen resistance. Her research team included study lead co-author Alexey Revtovich and co-author Ryan Lee.
"The key difference between the two diets is the ability of HT115 and OP50 to acquire B12 from the environment," said Revtovich, a research scientist. "We showed that HT115 is far more efficient at this, making about eight times as much of the protein that it needs to harvest B12 as compared to OP50."
The researchers used numerous tests to confirm their results and rule out other possible mechanisms for the effect. They also found that C. elegans on an HT115 diet had the ability to resist infection by another deadly human pathogen, Enterococcus faecalis.
Lee, a Rice undergraduate student, said the study highlights the need for C. elegans labs worldwide to pay attention to the possible differential impacts of diet on experimental outcomes.
"Some labs use OP50 as their standard food, and others use HT115 or even another strain of E. coli," Lee said. "Our results show there are significant metabolic differences between these diets, and it's likely those differences could contribute to substantial uncertainty in research outcomes."
abstract Diet is a crucial determinant of organismal biology; interactions between the host, its diet, and its microbiota are critical to determining the health of an organism. A variety of genetic and biochemical means were used to assay stress sensitivity in C. elegans reared on two standard laboratory diets: E. coli OP50, the most commonly used food for C. elegans, or E. coli HT115, which is typically used for RNAi-mediated gene knockdown. We demonstrated that the relatively subtle shift to a diet of E. coli HT115 had a dramatic impact on C. elegans’s survival after exposure to pathogenic or abiotic stresses. Interestingly, this was independent of canonical host defense pathways. Instead the change arises from improvements in mitochondrial health, likely due to alleviation of a vitamin B12 deficiency exhibited by worms reared on an E. coli OP50 diet. Increasing B12 availability, by feeding on E. coli HT115, supplementing E. coli OP50 with exogenous vitamin B12, or overexpression of the B12 transporter, improved mitochondrial homeostasis and increased resistance. Loss of the methylmalonyl-CoA mutase gene mmcm-1/MUT, which requires vitamin B12 as a cofactor, abolished these improvements, establishing a genetic basis for the E. coli OP50-incurred sensitivity. Our study forges a mechanistic link between a dietary deficiency (nutrition/microbiota) and a physiological consequence (host sensitivity), using the host-microbiota-diet framework.
Author summary
Vitamin B12 deficiency affects ~10–40% of US adults, causing a range of health issues ranging from anemia to neurological defects. Here we provide a mechanistic link between dietary B12 deficiency and mitochondrial dysfunction. Our data indicate that B12 supports clearance of propionate, an intermediate of branched chain amino acid metabolism. Excess propionate compromises mitochondrial homeostasis, increasing susceptibility to abiotic stresses and bacterial pathogenesis. Importantly, this deficiency is absent when worms are fed a diet of E. coli HT115. C. elegans reared on E. coli OP50 are predisposed to a variety of health defects, including increased sensitivity to bacterial pathogens and stresses; these subtle phenotypes may be difficult to recapitulate under conventional RNAi feeding conditions with HT115, introducing unexpected experimental confounds. These findings reinforce the importance of considering the host-microbiota-nutrient axis when using this model organism.
options for keeping the food system within environmental limits
marco springmann et al. 2018
http://dx.doi.org/10.1038/s41586-018-0594-0
feeding ten billion people is possible within four terrestrial planetary boundaries
dieter gerten et al. 2020
http://dx.doi.org/10.1038/s41893-019-0465-1
“When looking at the status of planet Earth and the influence of current global agriculture practices upon it, there’s a lot of reason to worry, but also reason for hope — if we see decisive actions very soon,” Dieter Gerten says, lead author from PIK and professor at Humboldt University of Berlin. “Currently, almost half of global food production relies on crossing Earth’s environmental boundaries. We appropriate too much land for crops and livestock, fertilize too heavily and irrigate too extensively. To solve this issue in the face of a still growing world population, we collectively need to rethink how to produce food. Excitingly, our research shows that such transformations will make it possible to provide enough food for up to 10 billion people.”
The researchers ask the question how many people could be fed while keeping a strict standard of environmental sustainability worldwide. These environmental capacities are defined in terms of a set of planetary boundaries — scientifically defined targets of maximum allowed human interference with processes that regulate the state of the planet. The present study accounts for four of nine boundaries most relevant for agriculture: Biosphere integrity (keeping biodiversity and ecosystems intact), land-system change, freshwater use, and nitrogen flows. Based on a sophisticated simulation model, the impacts of food on these boundaries are scrutinised at a level of spatial and process detail never accomplished before, and moreover aggregated to the entire planet. This analysis demonstrates where and how many boundaries are being violated by current food production and in which ways this development could be reverted through adopting more sustainable forms of agriculture.
Globally differentiated picture: In some regions, less would be more
The encouraging result is that, in theory, 10 billion people can be fed without compromising the Earth system. This leads to very interesting conclusions, as Johan Rockström, director of PIK points out: “We find that currently, agriculture in many regions is using too much water, land, or fertilizer. Production in these regions thus needs to be brought into line with environmental sustainability. Yet, there are huge opportunities to sustainably increase agricultural production in these and other regions. This goes for large parts of Sub-Saharan Africa, for example, where more efficient water and nutrient management could strongly improve yields.”
As a positive side effect, sustainable agriculture can increase overall climate resilience while also limiting global warming. In other places, however, farming is so far off local and Earth’s boundaries that even more sustainable systems could not completely balance the pressure on the environment, such as in parts of the Middle East, Indonesia, and to some extent in Central Europe. Even after recalibrating agricultural production, international trade will remain a key element of a sustainably fed world.
Hard to chew: Dietary changes needed
Importantly, there is the consumers’ end, too. Large-scale dietary shifts seem to be inevitable for turning the tide to a sustainable food system. For example, regarding China’s currently rising meat consumption, parts of animal proteins would need to be substituted by more legumes and other vegetables. “Changes like this might seem hard to chew at first. But in the long run, dietary changes towards a more sustainable mix on your plate will not only benefit the planet, but also people’s health,” adds Vera Heck from PIK. Another crucial factor is reducing food loss. In line with scenarios adopted in the present study, the most recent IPCC Special Report on land use found that currently, up to 30 percent of all food produced is lost to waste. “This situation clearly calls for resolute policy measures to set incentives right on both the producers’ and consumers’ ends,” Heck further lays out.
Perhaps the most sensitive and challenging implication of the study relates to land. “Anything involving land tends to be complex and contested in practice because people’s livelihoods and outlook depend on it. Transitioning to more sustainable land use and management is therefore a demanding challenge to policy-making. Key to success is that the regions affected need to see clear benefits for their development. Then there is a real chance that support for new directions will grow fast enough for stabilising the Earth system,” says Wolfgang Lucht, co-chair for Earth System Analysis at PIK and co-author of the study.
abstract Global agriculture puts heavy pressure on planetary boundaries, posing the challenge to achieve future food security without compromising Earth system resilience. On the basis of process-detailed, spatially explicit representation of four interlinked planetary boundaries (biosphere integrity, land-system change, freshwater use, nitrogen flows) and agricultural systems in an internally consistent model framework, we here show that almost half of current global food production depends on planetary boundary transgressions. Hotspot regions, mainly in Asia, even face simultaneous transgression of multiple underlying local boundaries. If these boundaries were strictly respected, the present food system could provide a balanced diet (2,355 kcal per capita per day) for 3.4 billion people only. However, as we also demonstrate, transformation towards more sustainable production and consumption patterns could support 10.2 billion people within the planetary boundaries analysed. Key prerequisites are spatially redistributed cropland, improved water–nutrient management, food waste reduction and dietary changes.
taste and smell
mammalian taste cells express functional olfactory receptors
bilal malik et al. 2019
http://dx.doi.org/10.1093/chemse/bjz019
taste and smell were considered to be independent sensory systems that did not interact until their respective information reached the brain. Ozdener was prompted to challenge this belief when his 12-year-old son asked him if snakes extend their tongues so they can smell.
In the study, published online ahead of print in Chemical Senses, Ozdener and colleagues used methods developed at Monell to maintain living human taste cells in culture. Using genetic and biochemical methods to probe the taste cell cultures, the researchers found that the human taste cells contain many key molecules known to be present in olfactory receptors.
They next used a method known as calcium imaging to show that the cultured taste cells respond to odor molecules in a manner similar to olfactory receptor cells.
Together, the findings provide the first demonstration of functional olfactory receptors in human taste cells, suggesting that olfactory receptors may play a role in the taste system by interacting with taste receptor cells on the tongue. Supporting this possibility, other experiments by the Monell scientists demonstrated that a single taste cell can contain both taste and olfactory receptors.
"The presence of olfactory receptors and taste receptors in the same cell will provide us with exciting opportunities to study interactions between odor and taste stimuli on the tongue," said Ozdener.
In addition to providing insight into the nature and mechanisms of smell and taste interactions, the findings also may provide a tool to increase understanding of how the olfactory system detects odors. Scientists still do not know what molecules activate the vast majority of the 400 different types of functional human olfactory receptors. Because the cultured taste cells respond to odors, they potentially could be used as screening assays to help identify which molecules bind to specific human olfactory receptors.
Moving forward, the scientists will seek to determine whether olfactory receptors are preferentially located on a specific taste cell type, for example, sweet- or salt-detecting cells. Other studies will explore how odor molecules modify taste cell responses and, ultimately, human taste perception.
abstract The peripheral taste and olfactory systems in mammals are separate and independent sensory systems. In the current model of chemosensation, gustatory, and olfactory receptors are genetically divergent families expressed in anatomically distinct locations that project to disparate downstream targets. Although information from the 2 sensory systems merges to form the perception of flavor, the first cross talk is thought to occur centrally, in the insular cortex. Recent studies have shown that gustatory and olfactory receptors are expressed throughout the body and serve as chemical sensors in multiple tissues. Olfactory receptor cDNA has been detected in the tongue, yet the presence of physiologically functional olfactory receptors in taste cells has not yet been demonstrated. Here we report that olfactory receptors are functionally expressed in taste papillae. We found expression of olfactory receptors in the taste papillae of green fluorescent protein-expressing transgenic mice and, using immunocytochemistry and real-time quantitative polymerase chain reaction experiments, the presence of olfactory signal transduction molecules and olfactory receptors in cultured human fungiform taste papilla (HBO) cells. Both HBO cells and mouse taste papilla cells responded to odorants. Knockdown of adenylyl cyclase mRNA by specific small inhibitory RNA and pharmacological block of adenylyl cyclase eliminated these responses, leading us to hypothesize that the gustatory system may receive olfactory information in the periphery. These results provide the first direct evidence of the presence of functional olfactory receptors in mammalian taste cells. Our results also demonstrate that the initial integration of gustatory and olfactory information may occur as early as the taste receptor cells.
bitter-induced salivary proteins increase detection threshold of quinine, but not sucrose
laura e martin et al. 2019
http://dx.doi.org/10.1093/chemse/bjz021
give that broccoli a chance.
Doing so won't just change your mind; it will actually change the taste of those foods, according to a new University at Buffalo study.
What sounds at first like a culinary parlor trick is actually a scientific matter based on specific proteins found in saliva. These proteins affect the sense of taste, and diet composition, at least in part, determines those proteins.
Saliva is a complex fluid containing around 1,000 specific proteins. Identifying all the players is a work in progress, but everything we eat is dissolved in saliva before it interacts with taste receptor cells and all these proteins are candidates for influencing stimuli before food is tasted.
"What you eat creates the signature in your salivary proteome, and those proteins modulate your sense of taste," says Ann-Marie Torregrossa, an assistant professor in UB's Department of Psychology and the associate director of the university's Center for Ingestive Behavior Research, a comprehensive research home for studying eating and drinking behavior, obesity and other factors contributing to the daily decisions people make related to food and fluid intake.
"We've shown in previous work with rats that changing your diet changes what proteins are in your saliva. Now we're showing that the proteins in your saliva change how you taste."
The findings, published in the journal Chemical Senses, have applications ranging from the obesity crisis to medical compliance.
"If we can convince people to try broccoli, greens and bitter foods, they should know that with repeated exposure, they'll taste better once they regulate these proteins," says Torregrossa.
How much repeated exposure? Give me a number.
"Our data doesn't provide a number, such as 12 servings of broccoli, however, for people who avoid these foods because of their bitterness, but would like to include them in their diet, they should know their taste will eventually change."
Bitterness is also a near-universal characteristic of many pediatric medicines, and getting infants to swallow a bitter liquid -- which by nature they want to reject -- can be a challenge.
"An additive to that medicine to make it less bitter would increase compliance," she says. "It's similar to liquid dietary supplements in the geriatric population, which often contain sugar to tame the bitterness. Achieving the same result without sweeteners has obvious benefits."
At a bare minimum, Torregrossa says health care and nutritional professionals can counsel people to explain the role of these salivary proteins.
"Trying to convince someone that a salad tastes great isn't going to work because to that person it doesn't taste great. Understanding with taste that we're dealing with something that's moveable is significant."
Think of this in an evolutionary context.
Bitter foods, for foragers, can serve as a sign of danger, but it's an unreliable predictor. Why look for another food source if there's something safe and abundant at hand?
"Instead of having the cognitive load of learning that a food is safe and having to maintain that memory, instead you know that eventually this bitter food will taste good," says Torregrossa. "It's an elegant physiological shift allowing you to put these foods into your diet."
For the study, Torregrossa trained to rats to choose from one of two water bottles after tasting a solution, to indicate whether it tasted bitter. Animal research in this case allows for tighter dietary control and the variation of specific proteins can be monitored in a way that's difficult to achieve with human participants.
"This is interesting because we're not asking, 'Do you like this?' we're looking only at 'Can you taste this as bitter?'" she says. "Animals with these bitter-induced salivary proteins turned on cannot taste the bitterness at higher concentrations than animals who do not have the same protein activated.
"Once these proteins are on board the bitter tastes like water. It's gone."
Torregrossa's work is an intriguing tactic in the obesity fight which sees many battles focusing on over-consumption of high-fat and high-sugar foods.
"The variation around sweets is very small," she says. "Nearly everyone likes a cupcake, but the variation around liking broccoli is enormous.
"This research helps explain why that variation with bitter food exists and how we can get more people to eat broccoli instead of cupcakes."
abstract Exposures to dietary tannic acid (TA, 3%) and quinine (0.375%) upregulate partially overlapping sets of salivary proteins which are concurrent with changes in taste-driven behaviors, such as rate of feeding and brief access licking to quinine. In addition, the presence of salivary proteins reduces chorda tympani responding to quinine. Together these data suggest that salivary proteins play a role in bitter taste. We hypothesized that salivary proteins altered orosensory feedback to bitter by decreasing sensitivity to the stimulus. To that end, we used diet exposure to alter salivary proteins, then assessed an animal’s ability to detect quinine, using a 2-response operant task. Rats were asked to discriminate descending concentrations of quinine from water in a modified forced-choice paradigm, before and after exposure to diets that alter salivary protein expression in a similar way (0.375% quinine or 3% TA), or 1 of 2 control diets. Control animals received either a bitter diet that does not upregulate salivary proteins (4% sucrose octaacetate), or a nonbitter diet. The rats exposed to salivary protein-inducing diets significantly decreased their performance (had higher detection thresholds) after diet exposure, whereas rats in the control conditions did not alter performance after diet exposure. A fifth group of animals were trained to detect sucrose before and after they were maintained on the 3% TA diet. There was no significant difference in performance, suggesting that these shifts in threshold are stimulus specific rather than task specific. Taken together, these results suggest that salivary proteins reduce sensitivity to quinine.
skipping breakfast concomitant with late-night dinner eating is associated with worse outcomes following st-segment elevation myocardial infarction
guilherme neif vieira musse et al. 2019
http://dx.doi.org/10.1177/2047487319839546
People who skip breakfast and eat dinner near bedtime have worse outcomes after a heart attack. That's the finding of research published today in the European Journal of Preventive Cardiology, a journal of the European Society of Cardiology (ESC).1
The study found that people with the two eating habits had a four to five times higher likelihood of death, another heart attack, or angina (chest pain) within 30 days after hospital discharge for heart attack.
This was the first study to evaluate these unhealthy behaviours in patients with acute coronary syndromes. Skipping breakfast was observed in 58%, late-night dinner eating in 51%, and both behaviours in 41%.
The study enrolled patients with a particularly serious form of heart attack called ST-segment elevation myocardial infarction (STEMI). "One in ten patients with STEMI dies within a year, and nutrition is a relatively inexpensive and easy way to improve prognosis," said study author Dr Marcos Minicucci, of São Paolo State University, Brazil.
He recommended a minimum two hour interval between dinner and bedtime. "It is said that the best way to live is to breakfast like a king," he added. "A good breakfast is usually composed of dairy products (fat-free or low fat milk, yogurt and cheese), a carbohydrate (whole wheat bread, bagels, cereals), and whole fruits. It should have 15 to 35% of our total daily calorie intake."
The study included 113 patients with a mean age of 60, and 73% were men. Patients were asked about eating behaviours on admission to a coronary intensive care unit. Skipping breakfast was defined as nothing before lunch, excluding beverages, such as coffee and water, at least three times per week. Late-night dinner eating was defined as a meal within two hours before bedtime at least three times per week.
Dr Minicucci noted that late-night dinner eating was defined by the two-hour interval between dinner and bedtime, rather than eating late at night. But nearly all participants with this habit were late-eaters.
Previous studies have found that people who miss breakfast and have a late dinner are more likely to have other unhealthy habits such as smoking and low levels of physical activity. "Our research shows that the two eating behaviours are independently linked with poorer outcomes after a heart attack, but having a cluster of bad habits will only make things worse," said Dr Minicucci. "People who work late may be particularly susceptible to having a late supper and then not being hungry in the morning."
"We also think that the inflammatory response, oxidative stress, and endothelial function could be involved in the association between unhealthy eating behaviours and cardiovascular outcomes," he added.
In this study, statin use before hospital admission was higher in the group with unhealthy eating habits and worse outcome. Dr Minicucci said: "There are some controversies regarding eating habits of patients using statins. Our study suggests that patients with STEMI perceive statins as an alternative path to health benefits. But these drugs should be an addition to healthy eating habits, not a replacement."
pre-hispanic fishing practices in interfluvial amazonia: zooarchaeological evidence from managed landscapes on the llanos de mojos savanna
gabriela prestes-carneiro et al. 2019
http://dx.doi.org/10.1371/journal.pone.0214638
A network of fish ponds supported a permanent human settlement in the seasonal drylands of Bolivia more than one thousand years ago, according to a new study published May 15, 2019 in the open-access journal PLOS ONE by Gabriela Prestes-Carneiro of Federal University of Western Para, Brazil, and colleagues. The study is the first to document the full range of fish species likely kept in these constructed ponds, and provides new insights into how humans modified the savannah environment to cope with the months-long droughts that characterize this region of the Amazon Basin.
The Llanos de Mojos region in central Bolivia is a vast plain which receives flooding rains from October to April, and then virtually no precipitation the rest of the year. Beginning about 500 AD, humans began to create monumental earthen mounds in the region, on which permanent settlements were established. One, called Loma Salavtierra, located more than 50 kilometers from the nearest major river, has become an important archaeological site. Previous work has established the existence of a series of shallow ponds rimmed by low earthen walls and connected by canals, which are believed to have captured rainfall and stored it throughout the dry season, potentially built to serve multiple purposes including water storage, drainage, and fish maangement.
In the current study, the authors conducted osteological and taxonomic identifications on the remains of over 17,000 fish found in midden piles at the site with the aid of a comparative collection. They identified more than 35 different taxa of fish, with four types of fish predominating: swamp-eels, armored catfish, lungfish, and tiger-fish, all of which are adapted to conditions of low oxygen and fluctuating water levels, as would be expected to arise in the ponds during the long dry period between annual rains.
Together with evidence of similar pond networks elsewhere in the region, the authors suggest that their results point to the use of these ponds for harvesting fish year-round, far from any rivers, permanent natural ponds, or other open-water habitat. Further studies will be needed to investigate fish storage and holding activities, and whether these activities changed in response to precipitation and landscape fluctuations.
The authors add: "The savanna, in contrast to the large Amazonian rivers, presents a distinct set of fishing habitats where humans likely established specific fishing strategies."
abstract Recent evidence suggests the existence of Pre-Hispanic fisheries in savanna areas of the Amazon basin. How these fisheries may have functioned is still poorly known. Although many studies have drawn attention to how Pre-Hispanic inhabitants of these savannas managed to deal with excess water, little attention has been paid to understanding how large and permanent populations were sustained during long periods of drought. In the Llanos de Mojos, one of the largest savannas in South America, the landscape is greatly affected by the impacts of annual, seasonal flooding and inundations, alternating with a dry period that can last 4–6 months. The fishing practices in this area were studied on the basis of analysis of more than 17,000 fish remains recovered at Loma Salvatierra, a monumental mound located in an interfluvial area 50 km from the Mamoré River and occupied between 500 and 1400 AD. In Loma Salvatierra, a network of circular walled ponds connected to a system of canals has been identified, raising questions about a possible use of these structures for fishing. The exceptional conservation of the bone material has enabled precise taxonomic identification of more than 35 taxa, the richest fish spectrum thus far documented in the Mojos region. The dominant fish, swamp-eels (Synbranchus spp.), armored catfishes (Hoplosternum spp.), lungfish (Lepidosiren paradoxa), and tiger-fish (Hoplias malabaricus) are characteristic of shallow and stagnant waters. Our work documents the first zooarchaeological evidence of a dryland, interfluvial fishing system in the Bolivian Amazon that incorporates distinct species and fishing practices, demonstrating that these regions contain year round resources. Research is taking its first steps toward understanding landscape modifications, fish environments, and specific cultural technologies employed on this and other lowland neotropical savannas that differ from those for fishing in open waters and rivers.
postprandial hyperglycemia stimulates neuroglial plasticity in hypothalamic pomc neurons after a balanced meal
danaé nuzzaci et al. 2020
http://dx.doi.org/10.1016/j.celrep.2020.02.029
The neuronal circuits in our brain governing feelings of hunger and satiety can modify their connections, thereby adjusting feeding behaviour to living conditions and maintaining a balance between food intake and calorie expenditure. Scientists suspect that this plasticity could be altered for obese subjects.
In a new study conducted on mice, a team led by Alexandre Benani, a CNRS researcher at the Centre for Taste and Feeding Behavior (CNRS/Inrae/University of Burgundy/AgroSup Dijon), has shown that these circuits are activated on the time scale of a meal, subsequently regulating feeding behaviour. However, this activation does not occur through a change in the circuit’s “connections.”
Scientists focused on POMC neurons in the hypothalamus, located at the base of the brain, which are known for limiting food intake. They are connected to a large number of neurons from other parts of the brain, with the connections of this circuit being malleable: they can be made and unmade very quickly based on hormonal fluctuations. Researchers observed that this neuronal circuit is not modified after a balanced meal, but that other nerve cells associated with POMC neurons, known as astrocytes, actually change form.
Astrocytes are star-shaped nerve cells that were first studied for their supporting role with respect to neurons. Under usual conditions, they sheathe POMC neurons and act somewhat like brake pads by limiting their activity. After a meal, blood glucose levels (glycaemia) temporarily increase, with astrocytes detecting this signal and retracting in less than one hour: once this “brake” is released, POMC neurons are activated, ultimately promoting the feeling of satiety.
Surprisingly, a meal that is high in fats does not lead to this remodelling. Does this mean that lipids are less effective in satisfying hunger? The scientists are trying to determine whether they trigger satiety through another circuit. It also remains to be seen whether sweeteners have the same effects, or whether they lure the brain by providing an addictive sensation of sweetness without satisfying hunger.
abstract •Postprandial hyperactivity of hypothalamic POMC neurons involves synaptic plasticity
•Postprandial plasticity of POMC neurons engages glial retraction
•Postprandial glial retraction around POMC neurons is triggered by hyperglycemia
•Glial retraction on POMC neurons modifies meal pattern
Mechanistic studies in rodents evidenced synaptic remodeling in neuronal circuits that control food intake. However, the physiological relevance of this process is not well defined. Here, we show that the firing activity of anorexigenic POMC neurons located in the hypothalamus is increased after a standard meal. Postprandial hyperactivity of POMC neurons relies on synaptic plasticity that engages pre-synaptic mechanisms, which does not involve structural remodeling of synapses but retraction of glial coverage. These functional and morphological neuroglial changes are triggered by postprandial hyperglycemia. Chemogenetically induced glial retraction on POMC neurons is sufficient to increase POMC activity and modify meal patterns. These findings indicate that synaptic plasticity within the melanocortin system happens at the timescale of meals and likely contributes to short-term control of food intake. Interestingly, these effects are lost with a high-fat meal, suggesting that neuroglial plasticity of POMC neurons is involved in the satietogenic properties of foods.
the hidden potential of urban horticulture
jill l. edmondson et al. 2020
http://dx.doi.org/10.1038/s43016-020-0045-6
green spaces including parks, gardens, allotments, roadside verges and woodland cover 45 per cent of Sheffield — a figure similar to other UK cities.
Allotments cover 1.3 per cent of this, while 38 per cent of green space comprised of domestic gardens, which have immediate potential to start growing food.
The interdisciplinary team used data from Ordnance Survey and Google Earth to reveal that an extra 15 per cent of the city’s green space, such as parks and roadside verges, also has potential to be converted into community gardens or allotments.
Putting domestic gardens, allotments and suitable public green spaces together would open up 98m2 per person in Sheffield for growing food. This equates to more than four times the 23m2 per person currently used for commercial horticulture across the UK.
If 100 per cent of this space was used for growing food, it could feed approximately 709,000 people per year their ‘five a day’, or 122 per cent of the population of Sheffield. But even converting a more realistic 10 per cent of domestic gardens and 10 per cent of available green space, as well as maintaining current allotment land, could provide 15 per cent of the local population — 87,375 people — with sufficient fruit and veg.
With just 16 per cent of fruit and 53 per cent of vegetables sold in the UK grown domestically, such a move could significantly improve the nation’s food security.
The study also investigated the potential for soil-free farming on flat roofs using methods such as hydroponics, where plants are grown in a nutrient solution, and aquaponics, a system combining fish and plants. These techniques could allow year-round cultivation with minimal lighting requirements, using greenhouses powered by renewable energy and heat captured from buildings, with rainwater harvesting for irrigation.
Flat roofs were found to cover 32 hectares of land in Sheffield city centre. While equivalent to just 0.5m2 per person, the researchers believe the high-yielding nature of soil-free farming means this could make a significant contribution to local horticulture.
The UK currently imports 86 per cent of its total tomato supply — but if just 10 per cent of the flat roofs identified within the centre of Sheffield became soil-free tomato farms, it would be possible to grow enough to feed more than eight per cent of the population one of their ‘five a day’. This increases to more than 60 per cent of people if three quarters of the flat roof area is utilised.
Dr Jill Edmondson, Environmental Scientist at the University of Sheffield and lead author of the study, said: “At the moment, the UK is utterly dependent on complex international supply chains for the vast majority of our fruit and half of our veg — but our research suggests there is more than enough space to grow what we need on our doorsteps.
“Even farming a small percentage of available land could transform the health of urban populations, enhance a city’s environment and help build a more resilient food system.”
Professor Duncan Cameron, co-author and Director of the Institute for Sustainable Food at the University of Sheffield, said: “It will take significant cultural and social change to achieve the enormous growing potential of our cities — and it’s crucial that authorities work closely with communities to find the right balance between green space and horticulture.
“But with careful management of green spaces and the use of technology to create distribution networks, we could see the rise of ‘smart food cities’, where local growers can support their communities with fresh, sustainable food.”
abstract Urban areas offer considerable potential for horticultural food production, but questions remain about the availability of space to expand urban horticulture and how to sustainably integrate it into the existing urban fabric. We explore this through a case study which shows that, for a UK city, the space potentially available equates to more than four times the current per capita footprint of commercial horticulture. Results indicate that there is more than enough urban land available within the city to meet the fruit and vegetable requirements of its population. Building on this case study, we also propose a generic conceptual framework that identifies key scientific, engineering and socio-economic challenges to, and opportunities for, the realization of untapped urban horticultural potential.
whole: rethinking the science of nutrition
t. colin campbell 2014
eating and healthy ageing: a longitudinal study on the association between food consumption, memory loss and its comorbidities
xiaoyue xu et al. 2020
http://dx.doi.org/10.1007/s00038-020-01337-y
high consumption of fruit and vegetables was linked to lowered odds of memory loss and its comorbid heart disease. High consumption of protein-rich foods was associated with a better memory.
Dr Xu also found the link between food group and memory status may vary among different older age groups. People aged 80 years and over with a low consumption of cereals are at the highest risk of memory loss and its comorbid heart disease, her research showed.
“Our present study implies that the healthy eating suggestions of cereals consumption in the prevention of memory loss and comorbid heart disease for older people may differ compared to other age groups,” said Dr Xu
abstract To explore the longitudinal association between food groups and memory loss and comorbid heart disease and diabetes (both Type 1 and 2) for people living in New South Wales, Australia.
Methods
We assessed 139,096 adults (aged 45 years and over) from the 45 and Up Study who completed both baseline (2006–2009) and follow-up (2012–2015) surveys. Mixed linear and generalized estimating equation models were used to examine the longitudinal associations.
Results
High consumption of fruit, vegetable and protein-rich food associated with lower odds of memory loss. High consumption of fruit and vegetables also associated with lower odds of comorbid heart disease (p ≤ 0.001). People who aged ≥ 80 years with low consumption of cereals had the highest odds of memory loss and comorbid heart disease than people in other age groups (p < 0.01).
Conclusions
The results highlighted the longitudinal association of fruit and vegetable in relation to memory loss and comorbid heart disease. Age effects on cereals consumption which have an influence on memory loss and comorbid heart disease.
hippocampal-dependent appetitive control is impaired by experimental exposure to a western-style diet
richard j. stevenson et al. 2020
https://doi.org/10.1098/rsos.191338
after seven days on a high fat, high added sugar diet, volunteers in their 20s scored worse on memory tests and found junk food more desirable immediately after they had finished a meal.
The finding suggests that a western diet makes it harder for people to regulate their appetite, and points to disruption in a brain region called the hippocampus as the possible cause.
“After a week on a western-style diet, palatable food such as snacks and chocolate becomes more desirable when you are full,” said Richard Stevenson, a professor of psychology at Macquarie University in Sydney. “This will make it harder to resist, leading you to eat more, which in turn generates more damage to the hippocampus and a vicious cycle of overeating.”

Previous work in animals has shown that junk food impairs the hippocampus, a brain region involved in memory and appetite control. It is unclear why, but one idea is that the hippocampus normally blocks or weakens memories about food when we are full, so looking at a cake does not flood the mind with memories of how nice cake can be. “When the hippocampus functions less efficiently, you do get this flood of memories, and so food is more appealing,” Stevenson said.
To investigate how the western diet affects humans, the scientists recruited 110 lean and healthy students, aged 20 to 23, who generally ate a good diet. Half were randomly assigned to a control group who ate their normal diet for a week. The other half were put on a high energy western-style diet, which featured a generous intake of Belgian waffles and fast food.
The Western-style diet is characterized by the consumption of highly processed and refined foods, high contents of sugars, salt, and fat and protein from red meat. It has been identified as a major contributor to the development of obesity-related diseases including type 2 diabetes, high blood pressure, and cardiovascular disease. The Western-style diet has also been associated with an increased incidence of chronic kidney disease.
At the start and end of the week, the volunteers ate breakfast in the lab. Before and after the meal, they completed word memory tests and scored a range of high-sugar foods, such as Coco Pops, Frosties and Froot Loops, according to how much they wanted and then liked the foods on eating them.
“The more desirable people find the palatable food when full, following the western-style diet, the more impaired they were on the test of hippocampal function,” Stevenson said. The finding suggests that disruption of the hippocampus may underpin both, he added.
Stevenson believes that in time governments will come under pressure to impose restrictions on processed food, much as they did to deter smoking. “Demonstrating that processed foods can lead to subtle cognitive impairments that affect appetite and serve to promote overeating in otherwise healthy young people should be a worrying finding for everyone,” he said. The work is published in Royal Society Open Science.
In the longer term, eating a western-style diet contributes to obesity and diabetes, both of which have been linked to declines in brain performance and the risk of developing dementia. “The new thinking here is the realisation that a western-style diet may be generating initial and fairly subtle cognitive impairments, that undermine the control of appetite which gradually opens the way for all of these other effects down the track,” Stevenson said.
Rachel Batterham, professor of obesity, diabetes and endocrinology at University College London, who was not involved in the study, said it was one of the first to investigate whether the western diet impairs memory and appetite control in humans.
“Understanding the impact of a western diet on brain function is a matter of urgency given the current food climate,” she said. “This research has provided data to support detrimental effects on both memory and appetite control after just one week of an energy-dense diet and may suggest a link between poor diet and impairment of the hippocampus, a key memory and appetite-associated brain region. The mechanisms at work remain to be elucidated and will require further research with the application of more sophisticated neuroimaging methods.”
abstract Animals fed a Western-style diet (WS-diet) demonstrate rapid impairments in hippocampal function and poorer appetitive control. We examined if this also occurs in humans. One-hundred and ten healthy lean adults were randomized to either a one-week WS-diet intervention or a habitual-diet control group. Measures of hippocampal-dependent learning and memory (HDLM) and of appetitive control were obtained pre- and post-intervention. HDLM was retested at three-week follow-up. Relative to controls, HDLM performance declined in the WS-diet group (d = 0.43), but was not different at follow-up. Appetitive control also declined in the WS-diet group (d = 0.47) and this was strongly correlated with HDLM decline (d = 1.01). These findings demonstrate that a WS-diet can rapidly impair appetitive control in humans—an effect that could promote overeating in consumers of a WS-diet. The study also suggests a functional role for the hippocampus in appetitive control and provides new evidence for the adverse neurocognitive effects of a WS-diet.
bbc recipe
bbc.co.uk/programmes/b080py3x
discussion thread
houzz.com/discussions/1728160/shark-fin-melon-patch-cucurbita-ficifolia
bread
panasonic breadmaking machine
sourdough process
petephillips.me.uk/blog/2018/03/sourdough-loaf-in-a-breadmaker/
sourdough starter
dovesfarm.co.uk/recipes/sourdough-starter
how we eat with our eyes and think with our stomach: the hidden influences that shape your eating habits
melanie mühl, diana von kopp 2017
the end of plenty: the race to feed a crowded world
joel bourne 2015
holy shit: managing manure to save mankind
gene logsdon 2010
food fight: gmos and the future of the american diet
mckay jenkins 2018
flavor: the science of our most neglected sense
bob holmes 2017
the gmo deception: what you need to know about the food, corporations, and government agencies putting our families and our environment at risk
sheldon krimsky, jeremy gruber 2016
kitchen mysteries: revealing the science of cooking
hervé this 2010
diet for a hot planet: the climate crisis at the end of your fork and what you can do about it
anna lappe 2010
eat for the planet: saving the world one bite at a time
nil zacharias 2018
the vegetarian myth: food justice and sustainability
lierre keith 2009
why you eat what you eat: the science behind our relationship with food
rachel herz 2017
the science of food: an exploration of what we eat and how we cook
marty jopson 2017
defending beef: the case for sustainable meat production
nicolette hahn niman 2014
science & cooking: a companion to the harvard course
michael brenner, pia sörensen, david weitz 2015
eating wildly: foraging for life, love and the perfect meal
ava chin 2014
eat the beetles!: an exploration of our conflicted relationship with insects
david waltner-toews 2017
against the grain: how agriculture has hijacked civilization
richard manning 2005
unsavory truth: how food companies skew the science of what we eat
marion nestle 2018
did you just eat that?: two scientists explore double-dipping, the five-second rule, and other food myths in the lab
paul dawson, brian sheldon 2018
the way we eat now: how the food revolution has transformed our lives, our bodies, and our world
bee wilson 2019
food diy how to make your own everything: sausages to smoked salmon, sourdough to sloe gin, bacon to buns
tim hayward 2013
the kitchen science cookbook
michelle dickinson 2019
tears in heaven
eric clapton
makiaea
would you know my name
if i saw you in heaven
would it be the same
if i saw you in heaven
i must be strong
and carry on
’cause i know / i don’t belong / here in heaven
would you hold my hand
if i saw you in heaven
would you help me stand
if i saw you in heaven
i’ll find my way / through night and day
’cause i know / i just can’t stay / here in heaven
time can bring you down
time can bend your knees
time can break your heart
have you beggin’ please
beggin’ please
(instrumental)
beyond the door / there’s peace i’m sure
and i know / there’ll be no more / tears in heaven
would you know my name
if i saw you in heaven
would it be the same
if i saw you in heaven
i must be strong
and carry on
’cause i know / i don’t belong / here in heaven
’cause i know / i don’t belong / here in heaven
chiquitita
abba
makiaea
chiquitita show me what’s wrong
I too have known such sorrow
through your eyes can you see hope for tomorrow?
how it hurts to see you like this
there is no way I can deny it
I can see that you’re oh so sad so quiet
chiquitita tell me the truth
my shoulder’s here to cry on
we’re best friends best friends you can rely on
though we’re mostly sure of ourselves
now and then we’ll break a feather
I hope we will grow new ones together
chiquitita you and I know
how the heartaches come and they go yet the stars keep shining
you’ll be dancing once again and the pain will end
the time will pass for grieving
chiquitita you and I cry
yet the sun is still in the sky and shines on above us
let me hear you sing once more like you did before
sing a new song chiquitita
try once more like you did before
sing a new song chiquitita
sing once more like you did before
sing a new song chiquitita
veg lacto pesce
cookbook.epub
paul’s fish soup via andi 20141020
olive oil, three tablespoons
onion, quarter–cup chopped
garlic, one teaspoon finely chopped
hot red pepper, half–cup chopped
leeks optional, half–cup chopped
carrots, half–cup finely chopped
red pepper, one crumbled
bay leaf, one
thyme, two teaspoons fresh chopped or half–teaspoon dried
white wine, one cup dry
tomatoes, one cup chopped fresh or canned
potatoes, one–third pound cubed
water, one cup
fish, one and a quarter pounds non–oily, white–fleshed such as cod or a combination of fish
bay scallops, half–pint
cream, one cup heavy
fresh parsley, quarter–cup chopped
salt and pepper
croutons optional, toasted
heat oil in pan, sautée onion, garlic, red pepper, leeks and carrots, stir often until onions wilt. meanwhile, chop potatoes and chill in cold water. to the pan, add bay leaf, thyme, wine and tomatoes. bring to boil. add rinsed potatoes.
cover loosely, cook ten minutes. add water, uncover, cook five minutes. add fish and scallops, cook two to three minutes, do not overcook or fish will fall apart.
add cream, bring to boil — make sure soup piping hot before serving. stir in parsley, add salt and pepper to taste. add croutons if desired, and serve.
non–veg
cookbook-2.epub
francium Fr (francia, france)
den lille pige med svovlstikkerne
(the little match girl)
HG
http link back to 00100
braun
raspberry ice cream (from braun)
serves: 2
100 g frozen raspberries
some raspberries for garnishing
20 g caster sugar
80 g cream
mint leaves
blend the frozen fruit with the caster sugar and cream in the large chopper of the multiquick hand blender for about 30 seconds at setting 3.
garnish with raspberries and mint and serve immediately.
ingredients
method
baked this in a metal saucepan lined with butter because our cake tins had not arrived from storage yet
chef luca
50 ml oil rapeseed
200 g tinned butter beans
250 g tinned borlotti beans
20 g garlic
2 g spice ground turmeric
4 g spice ground cumin
7 g ground coriander
1 g whole green cardamom
1g whole cloves
2 g cinnamon sticks
800 g tinned chopped tomato
15 g vegetable stock cube (knorr is best)
330 ml coconut milk
500 g onion medium
dilute the stock cube in 300 ml of hot water and set aside.
slice the onions and chop the garlic.
cook in oil for a couple of minutes.
add the spices and cook for a further minutes.
add the tomatoes and stock and cook for 10 minutes.
add the beans and coconut milk.
continue cooking for another 15 minutes.
happy cooking!! !
chef luca
silver spoon recipe
serves 4
2 tablespoons butter
generous 1/2 cup pancetta, diced
1 garlic clove
12 ounces spaghetti
2 eggs, beaten
1/2 cup parmesan cheese, freshly grated
1/2 cup romano cheese, freshly grated
salt and pepper
melt the butter in a pan, add the pancetta and garlic and cook until the garlic turns brown. remove and discard the garlic. meanwhile, cook the spaghetti in a large pan of salted, boiling water until al dente, then drain and add to the pancetta. remove the pan from the heat, pour in the eggs, add half the parmesan and half the romano and season with pepper. mix well so that the egg coats the pasta. add the remaining cheese, mix again and serve.
jenny (vegetarian) recipe
eggs, three
parmesan cheese, 3x4x1.5cm
garlic, one clove
sundried tomatoes, handful
porcini mushrooms, sliced handful dried or substitute pancetta (non–veg)
spaghetti, one packet
salt and pepper
olive oil, dash
soak porcini and sundried tomatoes in hot water, while boiling pasta
whisk eggs, add chopped porcini, tomatoes, garlic, add splash of milk, olive oil, salt and pepper to taste
when spaghetti cooked, drain and return to pan
on low heat, add mixture and stir until eggs cooked
bbc / good food 2005
1 tbsp olive oil
1 medium onion, chopped
2 celery sticks, chopped
2 tsp ground cumin
600ml hot vegetable stock
400g can chopped plum tomatoes with garlic
400g can chickpeas, rinsed and drained
100g frozen broad beans
zest and juice ½ lemon
large handful coriander or parsley and flatbread, to serve
heat the oil in a large saucepan, then fry the onion and celery gently for 10 mins until softened, stirring frequently. tip in the cumin and fry for another min.
turn up the heat, then add the stock, tomatoes and chickpeas, plus a good grind of black pepper. simmer for 8 mins. throw in broad beans and lemon juice, cook for a further 2 mins. season to taste, then top with a sprinkling of lemon zest and chopped herbs. serve with flatbread.
Link: instructables.com/id/How-to-make-REAL-Japanese-ramen-from-scratch/
Link: bakeforhappykids.com/2014/06/magic-custard-cake.html
daa2 hin3
tap and hold and roll side
grow vegetables from scraps
Link: healthy-holistic-living.com/17-plants-grow-kitchen-scraps.html
mnn.com/your-home/organic-farming-gardening/stories/how-to-regrow-food-from-scraps
cut this slice with sharp knife — this will reach room temperature more quickly and become spreadable