Showing posts with label Food. Show all posts
Showing posts with label Food. Show all posts

February 21, 2018

Korean Food: Revamped

The Olympics in South Korea are coming to an end on Sunday. If you got interested in the Korean culture and food, you definitely need to check out these restaurants in Berlin!

via Wikimedia Commons

Korean food has been taking Berlin by storm - it seems to be the trendy thing to enjoy nowadays - kimchi rolls, bulgogi (grilled meat) with a side order of mandu (dumplings), all washed down with some silky soju (rice liqour). If you do happen to be cool enough to be seen in these dining establishments, you are in "the know" of people who enjoy the gastronomic landscape of the city.
But it's not as if Korean restaurants are new to the scene: Gung Jeon for instance is a staple hang out amongst the Korean community, usually packed with expat or exchange students at lunch (with their secret lunch specials) with well beloved classic dishes which remind them of home - a warm bowl of seafood soup, a hearty plate of egg noodles with black bean sauce. Here, they serve the food straight up, with warm service and a homley atmosphere. It might be slightly intimidating for the non-Korean, as the clientele seems to already be in the know-how. German is hardly to be heard. Here, if you're a non-Korean, you must walk in with a poker face of confidence. "I know exactly what I am doing!"

Gung Jeon
Kurfürstendamm 134
10711 Berlin
+49 30 89541892
http://www.gungjeon.de/

Ixhthy's is the more grungy cousin of Gung Jeon - an Imbiss run by three Korean widows, blatantly pushing their Christian faith to every diner by wallpapering every possible inch with verses from the Bible. The Bibimbap - a popular dish amongst novices to Korean food - is exactly how it should be: sizzling hot, spicy to the point where your tongue hurts, and so delicious and satisfying from the generous serving of sesame oil and water spinach that you want to cuddle someone for an hour afterwards.
 Ixhthy
Pallasstrasse 21
10781 Berlin
+49 30 81474769
The new kids on the block take on a more sleek angle. Stylized décor, red lipsticked clientele with asymmetrical haircuts and an unseemly snooty gaze. This is the new Korean food scene in town. A well beloved establishment among this crowd of hipster joints is Kimchi Princess in Kreuzberg. Unmistakable Korean cookery is at work (I checked: the kitchen IS staffed with Korean cooks though I could have told you without having peeked), while the service staff is more international. The owner is half Korean himself, born in Germany. In a dimly lit high-ceilinged space with cool simple décor and red lighting, this is indeed the place to be nowadays. Just don't even think about walking in without having made a reservation first, and be aware that service on weekends can be slow from the many orders from packed tables. Kimchi Princess offers Korean food on steroids: delicious, sexy, young and hip. 
 Kimchi Princess
Skalitzer Str. 36
10999 Berlin, Germany
+49 163 4580203

By Gina Eom
This article originally appeared in Vol. 04 - Issue 3 - Brain Stimulation

January 12, 2018

Eat Well and Sleep Soundly, in These Two Good Health Abounds


Can Food Intake Influence Our Sleeping Pattern? There are few facts in life that are rock solid: food and sleep are among them. Everyone has to sleep - and obviously everyone has to eat. However, do these two fundamental pillars of bodily existence influence each other and if yes, in what way?

The WHY and WHEN of sleep is well studied and is known as the two-process-model of sleep-wake regulation. Process S is defined as a homogenic sleep drive which is generated by sleep inducing substances in the brain (WHY). Process C is the circadian clock, which serves as an internal time keeping device. It controls the timing of most of the processes in our body and by regulating “alertness”, it can influence WHEN we get tired.
The master clock in our brain (suprachiasmatic nucleus – SCN) can convey time cues (e.g., light-dark cycle) to the peripheral clocks which are ticking in almost every cell of our body. These in turn are thought to regulate local tissue physiology [1]. Now, this is where it gets interesting, since various metabolites can feed back onto the peripheral clocks and onto the SCN [2].
For instance, if food resources are restricted to a certain time of day, animals can go from being nocturnal to diurnal or vice versa on a behavioral level. This is also mirrored on the molecular level in tissues such as the liver [3, 4].



CHRONIC SLEEP DISRUPTION CAN LEAD TO OBESITY
 
Knowing how a system works means we can also trick it. For example, after a trans-continental flight, almost everyone suffers from jet lag. One way to adapt quicker is to eat meals corresponding to the local time, therefore already resetting our organ clocks to local time.
Conversely, if sleep rhythms and therefore eating rhythms are chronically disrupted, such as in shift workers, this can lead to obesity and other metabolic diseases [5].
All in all, in the hectic pace of modern life, we often neglect our body clocks concerning sleeping and food intake, thereby seriously endangering our health. As the medical psychologist Till Roenneberg said: "Time really is of the essence".

[1] Dibner et al, Annu Rev Physiol, 2010
[2] Morris et al, Mol Cell Endocrinol, 2012
[3] Damiola, Genes Dev, 2000
[4] Mistlberger, Eur J Neurosci, 2009
[5] Bass andTakahashi, Science, 2010

by Veronika Lang, PhD Alumna AG Kramer
This article originally appeared 2014 in CNS Volume 7, Issue 3, Nature vs Nurture

December 08, 2017

The Hypothalamus: Central Appetite Regulation


Feeding and energy expenditure are controlled by complex neural networks distributed throughout the forebrain and brainstem. Homeostatic feeding behavior is integrated within the hypothalamus. 

Key peripheral signals of energy status such as gut hormones and adipokines either signal to the hypothalamus directly or indirectly via the brainstem and vagal afferent fibres. Adiposity signals such as insulin and leptin are involved in the long-term energy homeostasis, and gut hormones such as ghrelin are implicated in the short-term regulation of meal ingestion [1-3]. The Hypothalamus comprises various nuclei, of which the arcuate nucleus (ARC), the paraventricular nucleus (PVN), the ventromedial nucleus (VMN), the dorsomedial nucleus (DMN), and the lateral hypothalamic area (LHA) play a role in energy homeostasis.


Hypothalamic Orexigenic and Anorexigenic Neuropeptides
The ARC, known as the infundibular nucleus in man, is situated at the base of the hypothalamus. It contacts the peripheral circulation through semi-permeable capillaries in the underlying median eminence and is thus in an ideal position to integrate hormonal signals for energy homeostasis. In the ARC, there are two important discrete neuronal populations: Neurons coexpressing neuropeptide Y (NPY) and agouti-related peptide (AgRP) stimulate food intake, whereas neurons coexpressing pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) suppress food intake. Both subpopulations project to the LHA and PVN, where they control the function of second-order neurons. In the PVN, two distinct subpopulations of neurons produce the anorexigenic (appetite-suppressing) neurotransmitters thyrotropin-releasing hormone, and corticotropin-releasing hormone. In contrast to this, in the LHA, two other subpopulations produce the orexigenic (appetite-stimulating) neurotransmitter orexin (hypocretin) and melanin-concentrating hormone (for review see [4, 5]).

Peripheral Hormones and Peptides Regulating Appetite
Leptin, predominantly synthesized in adipose tissue, inhibits NPY/AgRP neurons and stimulates POMC/CART neurons. Circulating leptin levels are directly proportional to adiposity in animals and humans. Insulin, which is produced in the β cells of the pancreas and rapidly secreted after a meal, binds to insulin receptors on the surface of POMC/CART neurons and activates them. The rise in circulating insulin in response to a glucose load is proportional to fat mass. Ghrelin, a hormone from the stomach, exerts a stimulating effect when binding at growth hormone secretagogue receptors on NPY/AgRP neurons. Circulating ghrelin decreases in response to chronic overfeeding and increases in response to chronic negative energy balance associated with exercise or anorexia nervosa. Whereas obese people usually have high plasma leptin, they have low plasma ghrelin (for review see [6]).

[1] Simpson et al., Arc Bras Endocrinol Metabol, 2009
[2] Stanley et al., Physiol Rev, 2005
[3] Suzuki et al., Endocr J, 2010
[4] Velloso et al., Neuroimmunomodulation, 2008
[5] Suzuki et al., Exp Diabetes Res, 2012
[6] Neary et al., Clin Endocrinol (Oxf.), 2004

By Charlotte Klein, PhD Alumna AG Neural Regeneration and Plasticity  
This article originally appeared 2012 in CNS Volume 5, Issue 4, Fat Gut or Fat Brain

December 06, 2017

Can You Be Addicted to Food?

Clearly, food is something that most people really cannot go without. For some, it is the casual craving for carbohydrate-rich food after a long, frustrating day, while others just enjoy Schnitzel too much. But in recent years, a growing controversy has developed from the question of whether there is a darker, more sinister side to the pleasure of eating. As an old Jewish proverb has it, "worries go down better with soup". But can drowning your sorrows in soup become a problem someday?

The concept of “food addiction” has been around for significantly longer than current debates may make you believe (nearly 60 years, to be precise) [1]. Conceptually, its location on the etiological food chain ranks it somewhere between substance (e.g. alcohol) and behavioral addictions (e.g. gambling). One reason why food addiction offers such an intuitive appeal is its seamless correlation with the global rise in obesity levels. Additionally, it offers a psychological remedy (a sugar-coating, if you excuse the pun) that relieves the consumer from the responsibility to choose: who could be blamed for overeating if all those companies sell food that has been carefully developed to maximize palatability and reward? However, the story may not be that straightforward.

Source: Bay Hippisley


As always when in doubt, a look at animal models proves instructive. And indeed, there is a plethora of studies indicating that animals often fall prey to developing addiction-like behavioral phenotypes when offered access to food. However, not all foods are created equal. More specifically, it has been shown that highly palatable foodstuff (so, the goodies that you should be careful with... you know, the ones with health warnings on them) including a high proportion of processed sugar, fat or salt, are especially attractive.

While it is generally appreciated that eating highly toothsome food activates reward areas and neurochemical paths that are notorious for their implication in addiction, it has remained significantly less clear whether this follows the act of eating per se, or depends on food content (i.e. certain ingredients). For instance, while there is evidence to suggest that lab rodents may show withdrawal-like symptoms when going cold turkey on sugar [2], such behaviors have generally not been described in humans (except in a single case study) [3]. For fat and salt, results have even been less clear.
Fast food is equivalent to pornography

Besides, there are some semantic problems that the term “food addiction” has difficulties digesting. Essentially, while no one debates the existence of problematic eating behavior, for instance, during binge eating attacks, the concept of addiction implies that there is something in the food that gets people hooked. However, humans who overeat tend not to be picky about a particular nutrient, but rather binge on a wide range of available toothsome foodstuff. And normally, there is very little evidence to suggest that humans ingest specific food to satisfy their craving for specific ingredients, like sugar or fat, or that these chemicals are consumed in isolation [4].

Eating addiction may be more appropriate than food addiction

From this perspective, ”addictive eating behavior” may be a better term. What is more, at this point, it has become challenging to tell apart people with increased appetite/reduced satiety from people with real “eating addiction” [4]. Overeating may, therefore, be something that is the consequence of high and readily availability of food paired with a certain vulnerability, such as negative effect, emotion dysregulation, and stress susceptibility [5]. To satisfy criteria for an addiction, rather than a maladaptive, potentially harmful behavior per se, science still has to carry forward the necessary proof. In any case, medicalizing such behavior may have its benefits, as has been the case for smoking, which today receives undivided medical/therapeutic attention. 

And while “food addicts” have been able to exchange their experiences among peers in Food Addicts Anonymous since 1987, they might have been the victims of a simple misnomer. For all those in doubt, better try the quiz at http://www.foodaddicts.org/am-i-a-food-addict.


[1] Randolph, Q J Stud Alcohol, 1956
[2] Colantuoni et al, Obes Res, 2002
[3] Thornley and McRobbie, N Z Med J, 2009
[4] Hebebrand et al, Neurosci Biobehav Rev, 2014
[5] Gearhardt et al, J Law Med Ethics, 2013

By Helge Hasselmann, PhD Student AG Otte

This article originally appeared September 2015 in Volume 08 Issue 02 "Food for Thought"

December 04, 2017

Are Oreos the New Cocaine?


We have all found ourselves reaching for that second delicious, crunchy Oreo (or maybe the German variant, Neo) after we finished the first one all too soon. But just because we do not stop with one cookie, does this mean we are addicted to them? Can Oreos be compared to drugs of abuse? Maybe. At least in rats.  

Source

Researchers at the University of Connecticut made headlines with their discovery that rats spent as much time in a chamber where they got Oreos as in one where they got a shot of cocaine or morphine. In other words, when rats had to pick between two chambers – one with a boring, bland, rice cake and one with an Oreo cookie – they preferred the Oreo chamber. And when given the choice between a shot of saline and a shot of morphine, they picked the morphine chamber. The researchers also found that eating cookies activated more neurons in the brain's nucleus accumbens than exposure to drugs of abuse [1]. 



EATING AN OREO GIVES US PLEASURE
Can we conclude that Oreos are as addictive as drugs of abuse? No! Here is a fatal flaw in the experiment: the researchers never directly compared Oreos to cocaine. They performed two independent experiments in two different groups of animals comparing rice cakes to Oreos and cocaine to saline. What the study does show is that eating an Oreo produces pleasure. But this is nothing new! In order to really find out if Oreos are as addictive as cocaine, we have to compare how hard a rat will work (for example, how often they press a lever) to get either an Oreo or a dose of cocaine [2]. Junk foods can create addictive-like tendencies [4] – this idea is neither new nor wrong. But the conclusions of this particular study certainly are [3].

How addictive are high fat/high sugar foods? Read the upcoming article to find the answer before checking into the treatment center for your addiction just yet!

[1] http://bit.ly/1KrTRTG
[2] http://bit.ly/1er5Fdp
[3] http://bit.ly/1MuWaIS
[4] Avena et al., Method Mol Biol, 2012


by Apoorva Rajiv Madipakkam
This article originally appeared 2015 in CNS Volume 8, Issue 3, Food for Thought.

October 30, 2017

A New Experience for the Adventurous Neuroscientist

In anticipation of Halloween, today's article is about an unusual type of meal.

When I heard that the MedNeuro newsletter was doing an issue on food and the brain, I naturally jumped at the chance to write an article. The excitement! The fun! The opportunity to explore a new frontier… in culinary arts. Yes, dear reader, this is an article all about cooking and eating brains.

But Are Brains Edible?
The short answer is “of course”! Like almost every other part of the body, the brain and spinal cord may be used from an animal to prepare various dishes. In fact, brain consumption in one form or another is practiced by groups worldwide. In Western Europe and North America, brain consumption is decreasing, as more desirable cuts of meat become more widespread and affordable. While you may not be able to find brain at the local Lidl or Netto, specialty butchers in Berlin will occasionally have calf brains for sale. Elsewhere in the world, brain still forms an important part of a traditional diet. For example, in Mexico, one can sometimes find “tacos de sesos”, while in parts of Indonesia, “gulai otak” (beef brain curry) is very popular.

Photo Giddy, "Brain Candy"

But Are Brains Safe to Eat?
In addition to changing demand for more “user-friendly” types of meat, brain consumption has decreased to concerns about its safety. Most readers are probably familiar with the string of deaths linked to Mad Cow (aka Creutzfeld-Jakob) Disease in the mid-1990s. This condition is still poorly understood, but is believed to stem from proliferation of prions in the brains and spinal cords of cattle that were fed remnants of other animals who died of the disease [1]. Humans who also ate meat from these animals became ill with neurological symptoms, and then swiftly died of generalized brain atrophy. Since the time of the first outbreak, most governments have taken aggressive steps to curtail the use of cattle byproducts as livestock feed, but cases still occasionally pop up every few years.

Consider yourself warned
 By and large, consumption of brain in Europe and North America should be relatively safe.
Another question of brain safety is worth mentioning, though is quite unlikely to apply to most would-be brain consumers: In the 1950s, a strange neurological disease was first noticed among the Fore region of Papua New Guinea. Eventually, the disease later christened “Kuru” was traced to practices of mortuary cannibalism, where family members of a recently deceased person would consume their remains in a gesture of respect. It was later determined to be another form of prion spongiform encephalopathy, much like Creutzfeld-Jakob [1]. These days, outbreaks are much more rare, but due to a long incubation period (2-20 years), cases still pop up [2]. So in case you are considering trying out human brain, consider yourself warned…

But Are They Good for You?
Ironically, brains are probably most dangerous in terms of their nutritional content. As any good neuroscientist knows, a good deal of the brain is formed by fatty myelin-covered axons. Thus, with small differences across species and methods of brain preparation, brain is extremely high in fat and cholesterol! For example, a serving of “pork brains in milk gravy” contains an estimated 1170% of daily-recommended cholesterol intake [3]! On the other hand, brains are also rich in omega fatty acids such as DHA [4]. All of this really takes “brain food” (see"The ABCs of Brain Foods - How to Eat Smart") to a whole new level.
Brain is extremely high in fat

But Are They Tasty?
The most important question of all! Although I’ve eaten some pretty “interesting” dishes in my life, I can’t say that I’ve ever (knowingly) tried brain. I’m a vegetarian, but I’m also quite curious. Hmmm… Perhaps the best thing to do is leave this here for exploratory purposes:

Swabian Brain Soup (Schwaebische Hirnsuppe)

Please note: The editors of the MedNeuro newsletter hold no responsibility for the safety, nutritional value, or tastiness of the following recipe suggestion!
Ingredients:
  • 1 onion
  • 2 tbs butter
  • 2 tbs flour
  • 750 ml water or beef stock
  • 1 tsp salt
  • 0.5 tsp grated nutmeg
  • 125 ml milk or cream
  • 2 tbs chopped parsley or chives
  • 1 egg yolk
  • 1 veal brain
Instructions:
  1. Rinse brain with hot water to remove blood and other connective tissue. Chop into small cubes.
  2. Peel and chop the onion. Saute with butter until golden-brown in a large pot and stir in flour. Pour in water/stock and simmer for 40 minutes. Add salt, nutmeg, and brain, and simmer for a further 10 minutes.
  3. Finally, add milk/cream, parsley/chives, and stir in the egg yolk. Serve soup hot with crusty bread.
Guten Appetit, and let us know how it goes!

[1] Wadsworth et al, PNAS, 2008
[2] Collinge et al, Philos Trans R Soc Lond B Biol Sci, 2008
[3] http://bit.ly/1g5qTPN
[4] http://bit.ly/1CVhbcw

by Constance Holman, PhD student AG Schmitz
This article originally appeared 2015 in CNS Volume 8, Issue 3, Food for Thought. 


October 27, 2017

Fasting: Cleansing of Spirit and Body?

Let’s face it: we live in a throwaway society and, in our daily lives, the longest period of food withdrawal lasts from dinner to breakfast the next morning. However, back when the word "globalization" did not exist, our ancestors used to undergo alternating periods of overfeeding and starvation, caused by fluctuating weather conditions and food availability. Fasting was a part of life. Nowadays, regular periods of fasting are still practiced around the world, but mainly for traditional, religious, or cultural reasons [1]. But what exactly are the effects of fasting on the brain and is it really healthy to fast? 

Source: Flickr


Fasting Comes in All Shapes and Sizes!
Before getting into the brain facts of fasting, let’s work a bit on terminology. Fasting is defined as abstaining from all kinds of food or drink and can last for short or extended periods of time, typically between 12 hours and 3 weeks [2]. Intermittent fasting is a type of fasting where you cycle between periods of fasting and non-fasting. In addition, fasting can also refer to abstaining only from selected foods, which usually lasts for longer time periods. On the other hand, starvation is defined as chronic nutritional insufficiency and although it is sometimes used synonymously for fasting, it generally describes more extreme forms [2].

Fasting: age less and be happier!

One example of short intermittent fasting is Ramadan, one of the best known religious fasting practices. Ramadan is the ninth month of the Islamic calendar during which Muslims don’t eat or drink from dawn to sunset [3]. Other fasting practices can be observed in several religions and range from abstinence from some or all kinds of food or drinks. Examples are Yom Kippur, the Day of Atonement in Judaism, when adults abstain from any food or drink for 24 hours [3], and fasting practices of the Greek Orthodox Christians, who forgo certain foods for a total of 180-200 days each year [4].

Effects on Our Bodies
While the purpose of religious fasting is primarily spiritual, it also has the potential to greatly affect one's physical health [4]. Prolonged fasting is a strong physiological stimulus and initiates a variety of responses in the body. Stunningly, intermittent fasting has been shown to enhance network plasticity, reduce oxidative stress and inflammation in the brain, increase neurotrophic factor availability and enhance stress resistance [2]. It is therefore not surprising that fasting is sometimes used in clinics: physicians monitor patients while they are fasting for periods lasting for one week or longer (usually only consuming water or a very low-calorie diet with less than 200 kcal/day) in order to improve weight management, disease prevention or treatment [2]. Fasting also seems to relieve various form of pain, ranging from non-specific chronic pain and fibromyalgia to migraines [5].

Lifting Up Your Spirits
Even more surprisingly, fasting doesn’t make you grumpy – on the contrary! Several studies have found that prolonged fasting is accompanied by increased alertness, better mood, a subjective feeling of being well and sometimes even euphoria [1]. One explanation for this could be an increase in tryptophan availability and serotonin turnover in the brain and the release of endogenous opioids [5].
Animal and human studies indicate that fasting – when done right, with the supervision of a professional – can have beneficial effects by reducing inflammatory markers and age-associated processes and be useful in the treatment of many different diseases [2].

[1] http://bit.ly/2vBPDqk
[2] http://bit.ly/2tpY7nY
[3] http://bit.ly/2u7PoUh
[4] http://bit.ly/2ua1XQJ
[5] http://bit.ly/2u7XkoT

by Juliane Schiwek, PhD Student AG Eickholt

This article originally appeared September 2017 in CNS Volume 10, Issue 3, Spirituality in Science


October 13, 2017

Our Intelligence Depends on Our Weight


The prevalence of obesity (defined as a Body Mass Index equal to or greater than 30) is increasing around the world. Medical doctors and investigators have long wondered if there is a link between obesity and brain disorders. 

Interesting observations were made regarding the age of obesity onset. Higher fetal and postnatal levels of adiposity contribute to better brain development. However, obesity in mid-life - at ages 40-55 - and during late-life - at age 70+ - increases risk for dementia, independent of education, IQ or other factors.
But what are the mechanisms by which obesity influences the brain and cognitive function? Adipose tissue may contribute to cognitive decline in a variety of ways. This may happen indirectly because obesity can cause diabetes or hypertension, leading to cardio- and cerebrovascular diseases that are able to impair cognitive function.

A more direct link is via adipokines. They can cross the blood-brain barrier and cause structural abnormalities, such as increased amounts of white matter. Leptin, produced mainly by adipose tissue, has remarkable effects on neurogenesis, neuroprotection, and regulation of beta-amyloid levels. Hereby, it is able to improve cognition, delay age changes, and optimize learning and memory processes. However, patients with common obesity can not benefit from elevated leptin levels because they show increased leptin resistance. A number of mechanisms, including the leptin-stimulated phosphorylation of Tyr(985) on LRb and the suppressor of cytokine signaling 3, attenuate leptin signaling and promote a cellular leptin resistance in obesity [1]. Another important multifunctional hormone is ghrelin. It is produced in a wide variety of tissues associated with the progression of obesity and metabolic syndrome. Acyl-ghrelin may modulate specific molecular intermediates involved in memory acquisition and consolidation through promotion of synaptic plasticity. In patients with Alzheimer's disease, the ghrelin autocrine/paracrine loop in the temporal lobe was found to be dramatically disrupted [2].

Furthermore, the brain can be susceptible to higher adiposity due to basic underlying differences in the structure and function of the nervous system. Studies using MRI have identified a number of brain regions potentially related to adult human obesity. These are mostly prefrontal areas which are different in gray matter density in obese and lean individuals. Higher BMI has also been related to a higher rate of brain atrophy using serial MRI [3].
It looks like exercise and maintaining a healthy weight are necessary not only to keep ourselves fit, but also to keep our brains functioning well.

[1] Paz-Filho G, Int J Clin Pract, 2010
[2] Gahete M et al., Peptides, 2011
[3] Enzinger C et al., Neurology, 2005

By Natalia Denisova, MSc Student Medical Neurosciences  

Tis article originally appeared December 2012 in Volume 05, Issue 04, Fat Gut or Fat Brain

October 11, 2017

The Fat Brain or the Fat Gut


Today is world obesity day. While we featured already several articles about obesity (Big, Bigger, Obese), dieting (Dieting and the Brain), other ways to loose weight (HCG Injections for Weight Loss) and ideal nutrition (How to Eat Smart), today's article gives a great introduction about the relationship between the brain and the gut and how  it is associated with obesity
 

Obesity - A Burden to Modern Society
Obesity has become one of the major challenges to human health worldwide, most markedly in industrialized countries. In Germany, about half of the adult population is classified as being overweight or obese, with a higher percentage in males (60 %) than in females (44 %) (GEDA, Robert Koch Institute, 2010). Overweight or obese individuals have a high risk of developing comorbidities, including type II diabetes mellitus, hypertension, and coronary heart disease, the most common cause of premature mortality in the obese population.
Body mass stability largely depends on the perfect coupling between caloric intake and energy expenditure [1]. Obesity is a state in which energy intake chronically exceeds energy expenditure. Even a subtle mismatch (less than 0.5 %) in caloric intake over expenditure is sufficient to cause weight gain [2]. The rising prevalence of obesity is likely due to contemporary environmental and lifestyle factors, such as overconsumption of energy-dense food and reduced requirements for physical activity in comparison with the lifestyle of our hunter-gatherer ancestors.

Who is to Blame?

The Brain and the Egg-and-Chicken Principle
The role of the hypothalamus in the regulation of feeding and energy balance was first highlighted by lesion studies in rodents [3, 4]). This brain area comprises specialized neurons that modulate food intake by acting to either stimulate or -suppress appetite (see article by Charlotte Klein). Because of this, the hypothalamus has been determined as a key component in the regulation of metabolic homeostasis "integrating information regarding the body's internal environment and orchestrating a series of coordinated endocrine, autonomic, and behavioral responses that maintain metabolic homeostasis" [5]. However, while great efforts have been made to understand how the brain controls our desire to feed as well as the processes underlying the balancing of energy intake and expenditure, little is known about how the structure and organization of the hypothalamus are altered by obesity. The question still remains whether obesity is a consequence of hypothalamic dysfunction or if it even causes changes in the functionality of the hypothalamus, as has been observed in rodent studies of obesity.

The Role of the Intestinal Tract
Not only the brain, but also the gut takes part in the regulation of appetite and fat storage. There is a long list of factors that originate from the gastrointestinal system and play a role in the management of energy balance by regulating the satiety feeling and thereby, food intake. The main ones are ghrelin, cholecystokinin, peptide YY, pancreatic peptide, glucagon-like peptide 1, and oxyntomodulin (for reviews [6] and [7]).
But these are not the only 'gut factors' controlling energy homeostasis of our organism. Recently, another key player was added to the regulators of our energetic well-being: the intestinal microbiota. These microorganisms, living in our gastrointestinal tract, have coevolved with their human hosts through ages, becoming important for many processes in the human body (see article by Sophie Schweizer). Actually, one could say, we are more microbes than man, because the number of bacterial cells in our intestines exceeds the number of the human cells in our body. Would you believe that the intestinal bacteria have an estimated mass of 1 to 2 kilogram? [9]
It has been shown in studies in mice and humans that the composition and function of microbiota may play a crucial role in the regulation of fat storage and lipid metabolism (more to be read in the article by Jana Foerster). Commensal microorganisms also seem to play a role in some obesity-related comorbidities, for example type II diabetes. Jens Nielsen, at the METAHIT conference in Paris in 2012, even stated that: "Gut microbiota species abundance is a more accurate predictor of type II diabetes than waist-to hip ratio".
Very interesting data have been produced by studies using germ-free mice (animals raised with zero contact to bacteria, see also article by Katarzyna Winek). These mice are leaner than their wild-type littermates, who have about 40 % more fat tissue. After colonization with bacteria from conventionally raised mice, the previously germ-free animals start to gain weight despite decreasing food consumption [10]!

Then, is it the Microbiota Issue?
It is good to take care of our microbial friends: A recently published Nature paper from the group of Martin Blaser describes how subtherapeutic doses of antibiotics can influence the metabolism. They created an adiposity model by introducing antibiotic low-dose treatment. Investigated animals had changes in their microbiome composition and alterations in many metabolic pathways [11]. Another interesting study showed decreased diversity and overall number of gut microbiota in the populations with a high prevalence of severe obesity and its related diseases. Additionally, the most effective obesity treatment (a surgical intervention by gastric banding, sleeve gastrectomy or gastric by-pass, used only in the most severe cases, i.e. BMI ≥ 40) not only leads to improvement in the inflammatory and hormonal status, but also to changes in the gut microbiome. However, up to now only limited data have been produced [12].

Better be Good to Your Commensal Bacteria!

We may say with certainty that we have not yet unraveled all the connections between the gut, the microbiota and the brain or their particular roles in the pathogenesis of obesity, but understanding this signaling in obesity and associated diseases is of huge importance. Recent discoveries and detailed characteristics of pathways involved in the pathogenesis may lead to more effective therapies with multiple targets. It is probably neither the brain nor the gut alone, but a complex interaction of both to blame for round shapes.


[1] Morton et al., Nature, 2006
[2] Hagan and Niswender, Pediatr Blood Cancer, 2012
[3] Tepperman et al., Yale J Biol Med, 1943
[4] Stellar, Psychol Rev, 1954
[5] Williams et al., Eur J Pharmacol, 2011
[6] Small and Bloom, Trends Endocrinol Metab, 2004
[7] Suzuki et al., Exp Diabetes Res, 2012
[8] Murphy and Bloom, Exp Physiol, 2004
[9] Forsythe and Kunze, Cell Mol Life Sci, 2012
[10] Bäckhed et al., Proc Natl Acad sci U S A, 2004
[11] Cho I et al., Nature, 2012
[12] Aron-Widnewsky et al., Nat Rev Gastroenterol Hepatol, 2012

By Charlotte Klein and Katarzyna Winek, PhD Students Medical Neurosciences  

Tis article originally appeared December 2012 in Volume 05, Issue 04, Fat Gut or Fat Brain

August 18, 2017

Resisting Temptations and the Power of Suggestion

Have you ever struggled to resist a delicious chocolate bar while you were on a diet? Or have you tried to resist drinking the sixth tequila shot which you knew would make you feel miserable the next day? Resisting temptations is difficult. However, a recent study published in Social Cognitive & Affective Neuroscience indicates that there are methods to help you.

Our research team at the Charité hypothesized that hypnotic suggestions and/or autosuggestions (giving suggestions to oneself) may be able to reduce the attractiveness of unhealthy temptations, or more specifically, snack food.
We invited 32 participants who were responsive to hypnosis and assigned them to two groups. One group was hypnotized by a professional hypnotist, while the other group used autosuggestion. Participants in the hypnosis group were suggested to experience disgust whenever they would encounter a color cue after hypnosis, namely green (half of the participants) or blue (the other half). They were further suggested that they would experience disgust only regarding specific snacks, namely either sweet snacks (half of the participants) or salty snacks (the other half). This was done to assess if hypnosis can target specific stimuli, rather than merely inducing a general feeling of disgust. In the autosuggestion group, participants were instructed to make the disgust association (regarding specific snacks and the cue color) on their own, and they were given as much time for this as the hypnotized participants. Afterwards, participants entered a functional magnetic resonance imaging (fMRI) scanner and carried out a virtual auction on sweet and salty snacks (e.g. Mars bars, Snickers bars). These snacks were shown on a background that was blue for half of the time and green for the rest of the time.

Experimental procedure and the paradigm used in the scanner. Source: Ludwig et al, Soc Cogn Affect Neurosci, 2013


We found that participants of both groups were less willing to pay for the snacks targeted by hypnosis or autosuggestion (salty or sweet) when shown on the relevant cue color (blue or green background, depending on the participant). Surprisingly, there were no behavioral differences between the hypnosis and the autosuggestion group. Also, on a self-report questionnaire, participants of both groups indicated that they had indeed experienced disgust regarding the targeted snacks. However, participants subjected to hypnosis described the effects as more automatic, physical, and genuine (not merely simulated) compared to participants who had used autosuggestion. Finally, the fMRI data analysis showed that the ventromedial prefrontal cortex (vmPFC) was activated less when participants (in both groups) made decisions about targeted snacks shown on the cue color compared to the other snacks. The vmPFC is known to correlate with the perceived attractiveness of stimuli. Thus, the fMRI data are consistent with the idea that the targeted snacks were indeed perceived as less attractive than the other types of snacks following the interventions. Interestingly, hypnosis affected vmPFC activation more than autosuggestion.

Effects on VMPFC were stronger in the hypnosis group compared to the autosuggestion group. Source: Ludwig et al, Soc Cogn Affect Neurosci, 2013


In sum, both hypnosis and autosuggestion can decrease the attractiveness of unhealthy snacks. Moreover, neural and self-report evidence indicate that hypnosis has stronger effects than autosuggestion. Future studies should test the longevity of these effects and should determine whether the differences in brain activation and self-report between the groups are relevant for real-life behavior. The next time you want to resist chocolate, take some time to relax and suggest to yourself that it is disgusting - you might be surprised how powerful a suggestion can be.

Reference
Ludwig et al, Soc Cogn Affect Neurosci, 2013

By Dr. rer. nat. Vera Ludwig, Postdoctoral Fellow, Divison of Mind and Brain Research at the Charité.
this article was originally published 2014 in CNS Volume 7, Issue 1, Mind and Brain 

June 03, 2017

The ABCs of Brain Foods - How to Eat Smart

Planning a picnic during the long weekend, but not sure what to put in picnic basket? Here is a list of healthy foods with lots of benefits for your brain.

A: Amino acids:
Your body cannot synthesise all of the 20 amino acids. Nine of them can only be obtained through food, including tryptophan and phenylalanine. These two amino acids, along with tyrosine, are the biosynthetic precursors for the neurotransmitters serotonin, dopamine, and norepinephrine. The amino acids glutamate and aspartate are themselves neurotransmitters as well. However, they are not taken up into the brain from the diet. Regular meals containing aspartate and glutamate have no effect on the levels of these neurotransmitters in the brain. The brain is only affected when glutamate is administered alone in extremely large doses [1]. Meat, fish, eggs, dairy products and legumes are rich in protein and thus, amino acids.

B: B complex vitamins
A typical component of dietary supplements for the brain are vitamin B complexes, which include Vitamin B6, B12 and folic acid. Vitamin B6 is a cofactor in the production of cysteine and vitamin B12 is a cofactor needed in folic acid metabolism. Folate promotes the regeneration of methionine from homocysteine. They all work by reducing levels of homocysteine and their deficiency leads to hyperhomocysteinemia. This can lead to DNA damage, increase the generation of reactive oxygen species, contribute to excitotoxicity and cause mitochondrial dysfunction which may lead to apoptosis [2]. Further, vitamin B12 deficiency and high levels of homocysteine double your risk for brain atrophy and cognitive decline [3, 4]. Taking vitamin B6, B12, and folic acid can reduce brain atrophy and improve brain function [5]. Vitamin B6 can be found in dairy products, meat and fish, but also in cabbage, beans, whole meal products, nuts, yeast, avocados and bananas. Foods with high folate content are dark green leafy vegetables like spinach, avocado, liver, asparagus, brussel sprouts, nuts, beans, dairy products and eggs. Animal products are the best source of vitamin B12; you find it especially in liver, but also in eggs and dairy products. For vegans it is difficult to get enough B12. A recent study suggests that dried purple laver (Nori) could be a good source of B12 for vegans and vegetarians [6].
Brainfoods by Claudia Willmes

C: Calcium
This is one of the most important messengers in neurons. Indeed, only a few neuronal functions are immune to the influence of calcium! A transient rise in cytoplasmic calcium concentration allows activation of a large number of Ca2+-binding proteins that start signalling cascades. As calcium participates in the transmission of the depolarizing signal and contributes to synaptic activity, calcium deficiency impairs many neurological functions. Milk and dairy products as well as green vegetables, sesame seeds and nuts are an excellent source of calcium.

C: Chromium
Chromium is a trace mineral found in many nutritional supplements, especially in weight-loss and muscle-building pills. The use of chromium-containing dietary supplements is controversial, owing to the absence of any verified biological beneficial effect on healthy people [7]. However, eating some chromium should not hurt. Food sources of chromium are broccoli, grapes, whole-wheat products and potatoes.

F: Fat
Many people avoid eating fat because they are afraid of gaining weight, but never underestimate their necessity for a functioning brain! Fatty acids are structural components of myelin. Both prenatal and postnatal fatty acid deficiency in rodents reduces the amount and alters the composition of myelin [8]. Avocado, olives and coconut oil are an excellent source of essential fatty acids. Very often, omega 3 fatty acids are found in dietary supplements. There are two main omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The latter shields against age-related mental decline and improves both learning and memory in older adults [9]. People with low DHA levels actually have smaller brains and exhibit more cognitive impairment than those with adequate levels [10]! The best sources of omega-3 are animal products: cold-water fish such as salmon, as well as dairy products from animals on a grass-fed diet. Plants only contain the fatty acid precursor alpha-linolenic acid (ALA), of which a tiny amount eventually gets converted to EPA and DHA in the body. If you are vegan, eat pumpkin seeds, walnuts, soy beans and seaweed.

G: Glucose
This is the second important addition in neuro-drinks and the brain's primary energy source. Blood glucose levels influence mood and attention span. Glucose administration also improves performance in cognitively demanding tasks [11]. The brain cannot store glucose and needs a steady supply, but this does not mean you should constantly be sipping soda! To ensure a constant glucose supply to your brain, eat food with high fiber carbohydrates such as carrots, beets, potatoes or dark fiber-rich whole wheat bread.

I: Iodine
The body cannot produce iodine, so it is an essential part of your diet. This trace element is required for producing thyroid hormones [12] which, in turn are required for brain development. Iodine deficiency in utero or during early postnatal development results in impaired cognitive and motor development [12]. Pregnancy, smoking and increased alcohol intake are risk factors for iodine deficiency. Great sources for iodine are saltwater fish and seafood, milk and dairy products, and, of course, iodized salt.

I: Iron
Iron is an important mineral for neurodevelopment and neuronal function. It plays a fundamental role in neurotransmitter synthesis, myelination and ensures oxygenation and energy production in the brain. Iron deficiency appears to alter the metabolism of the monoamines dopamine and norepinephrine [13] and decreased iron intake is associated with reduced myelination [14]. Iron deficiency is linked to attention-deficit/hyperactivity disorder and abnormal development of cognitive functions. Iron deficiency is particularly common in women and is associated with depression [15]. Rich sources of dietary iron include red meat, fish, legumes such as lentils and chickpeas, leafy vegetables and whole-grain products.



M: Magnesium
Magnesium is often listed as a supplement in brain-boosting drugs or drinks. It is involved in all the major metabolic pathways such as oxidation-reduction and ionic regulation. It also blocks the NMDA receptor, thereby preventing glutamate excitotoxicity. In magnesium deficiency, NMDA receptors become hyperexcitable, leading to excessive intracellular calcium. This can cause production of toxic reactive oxygen species and eventually lead to neuronal cell death. People with low magnesium are more susceptible to migraine attacks [16]. Parkinson's patients have low magnesium levels in the brain and rats with chronic low magnesium rapidly lose dopaminergic neurons [16]. Supplementary magnesium may thus be beneficial to prevent Parkinson's disease. Increased magnesium intake can also lead to improvement in patients with mania and depression [16]. The exact benefit of magnesium supplementation however is not yet definitive. Although whole grains contain magnesium, phytic acid in grains can inhibit its absorption. Therefore, the best sources of magnesium are dairy products, beans, leafy green veggies, and nuts.

V: Vitamin C:
This is an important antioxidant, serving as an electron donor in biological reactions. The brain has higher concentrations of Vitamin C compared to other organs [17]. It participates in neuronal maturation and myelin formation and supplies electrons for dopamine-β-hydroxylase, catalyzes the formation of norepinephrine from dopamine and is involved in presynaptic re-uptake of glutamate. Thus, it modulates the cholinergic, catecholinergic, and glutamergic systems [17]. Studies show that vitamin C levels are low in patients with dementia while research with animal models show that vitamin C supplementation can reduce cognitive decline [18]. Foods rich in vitamin C are citrus fruits, berries, bell peppers and sea buckthorn.

V: Vitamin D:
Although it's difficult to obtain from food, one thing you should definitely not get too little of is vitamin D. The best food source by far is cod liver oil (yuck!). Luckily, vitamin D is created when our skin is exposed to sunlight. Vitamin D has profound effects on the brain during all stages of life. Continuing to get adequate vitamin D throughout adult life can ward off cognitive decline, dementia, and Alzheimer’s disease [19, 20].

W: Water:
Obviously the most important thing for your brain is water. It helps the blood flow and consequently the oxygen supply of the brain. Thus, our advice: Try to drink 2 liters of water per day.

Z: Zinc:
The organ containing the highest amount of zinc is the brain, especially the hippocampus and cerebral cortex. Zinc acts as an antagonist of the NMDA receptor, induces BDNF gene expression and is a cofactor in the conversion of homocysteine to cysteine. Early postnatal zinc deficiency impairs neurogenesis, leading to learning and memory deficits persisting into adulthood [21]. Studies with rodent depression models and clinical studies have demonstrated the benefit of zinc supplementation in antidepressant therapy [22]. In animal models of depression, zinc treatment has antidepressant-like effects and dietary zinc insufficiency induces depressive behaviors [23].  Even though zinc has been associated with many psychological disorders, the nature of this relationship remains unclear. Seafood, beef, lamb, "variety meats" such as liver or brain, and some cheeses such as Emmental, Edam and Gouda are excellent sources of zinc. Plants provide us with zinc as well, but with lower bioavailability. Vegetarians and vegans should consume seeds, nuts, spinach, cocoa and beans to get enough zinc.

Our advice: Add these smart foods to your shopping list and go out for a picnic in the sun!

[1] Fernstrom, J Am Diet Assoc, 1994
[2] Kronenberg, Curr Mol Med, 2009
[3] de Jager, Neurobiol Aging, 2014
[4] Tangney et al, Neurology, 2011
[5] Douaud et al, PNAS, 2013
[6] Watanabe et al, Nutrients, 2014
[7] EFSA Panel, EFSA Journal, 2014
[8] Salvati et al, Dev Neurosci, 2000
[9] Yurko-Mauro et al, Alzheimers, 2010
[10] Tan et al, Neurology, 2012
[11] Brandt et al, Behav Neurosci, 2013
[12] Delange, Proc Nutr Soc, 2000
[13] Burhans et al, Nutr Neurosci, 2005
[14] Todorich et al, Glia, 2009
[15] Lozoff et al, Semin Pediatr Neurol, 2006
[16] de Baaij et al, Physiol rev, 2015
 [17] Normann Hansen et al, Nutrients, 2014
[18] Harrison et al, Nutrients, 2014
[19] Lee et al, J Neurol Neurosurg Psychiatry, 2009
[20] Anastasiou et al, J Alzheimers Dis, 2014
[21] Chowanadisai, J Neurochem, 2005
[22] Nowak et al, Pharmacol Rep, 2005
[23] Swardfager et al, Neurosci Biobehav Rev, 2013

by Claudia Willmes, PhD Student AG Eickholt / AG Schmitz
This article originally appeared 2015 in CNS Volume 8, Issue 3, Food for Thought.

March 20, 2017

HCG Injections for Weight Loss - Tricking The Brain or Tricking Your Wallet?


Spring is coming, and so is the urge to get fit and healthy. We know that the best way to get fit and healthy is through exercise and optimal nutrition, but wouldn't it be nice to reach your goals faster with the help of medicine?

A growing trend in popular culture has been the use of HCG (human chorionic gonadotropin) as treatment for obesity. First touted in the early 50’s by Dr. Albert Simeons as a miracle cure that, in combination with a strict 500 kcal/day diet, leads the body to preferentially burn stored fat rather than muscle, while tricking the brain into feeling neither hungry, irritable, nor fatigued. In a 1954 paper, Simeons claims to have treated 500 patients for 40 days, all of whom lost between 9-14 kg while maintaining a sense of well-being [1]. But what is HCG exactly, and is this regimen healthy or even effective?

Fat Profits by Mike Licht via Flickr


HCG, a commonly occurring hormone during pregnancy, can be extracted from the urine of pregnant women and is approved for the treatment of various forms of infertility [2]. However, many online pharmacies have begun marketing it for weight-loss, infusing it with vitamin B12, and charging an astronomical 200-250€ for a month’s supply [3].
Still, international authorities including the FDA have issued statements that HCG provides no benefit in the treatment of obesity, which is unsurprising given its paucity of clinical trials [1]. Authors of a 1995 meta-analysis of 24 clinical trials also concluded that “there is no scientific evidence that HCG is effective in the treatment of obesity; it does not bring about weight loss or fat redistribution, nor does it reduce hunger or induce a feeling of well-being” [2]. In fact, an alarming number of studies have reported adverse effects of the hormone including blood clots, headaches, restlessness, depression, and dizziness [1]. Last year, a case report was published on a 32-year-old female who suffered a manic episode as a result [4].

HCG PROVIDES NO SOLUTION TO TREAT OBESITY

The conclusion? A diet of 500 kcal/day will induce significant weight loss, but HCG neither “tricks” the brain nor augments the diet’s overall effect. Furthermore, it fails to provide the body with necessary nutrition and can lead to deficiencies and imbalances that negatively impact the brain.

[1] Robb-Nicholson, Harvard Women's Health Watch, 2010
[2] Lijesen et al, Br J Clin Pharmacol, 1995
[3] nuimagemedical.com
[4] Sanches et al, Bipolar Disord, 2014

by Kristina Kelly
This article originally appeared September 2015 in Volume 08 Issue 02 "Food for Thought"