Sweeteners Increase the Sweetness Threshold Required to Satisfy Your Sweet Tooth - Human Study Makes it Official! Overeating Still Not Necessarily an Issue For Most of Us

Evil or harmless? If you exert some self- control, the effects non-nutritive natural and artificial sweeteners are about to have on the amount of sweetness it takes to satisfy you is not enough to make you fat - I mean, you are no fattening pig, but an intelligent human being with a free will and a decent degree of self-control.

Some of you may have seen my post an a recent sweetener review in the SuppVersity Facebook News, already. In said post, I mention that Katharine Mary Wright makes the same proposal I did in a previous article on artificial sweeteners: the possibility of getting used to the intense sweetness could be, even if the sweeteners are non-toxic and non-insulinogenic, an issue we should not discard lightly. After all, someone who has been consuming his coffee with a ton of stevia for years is not likely to notice the calorie overload, when he happens to drink one the sugar-monsters at Starbucks.

That being said, my rationale has hitherto been based on the assumption that this accommodation effect will even occur. Today, a couple of months after I first issued my hypothesis, I have a study from the  Texas Christian University to prove it.

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In a series of experiments, Sarah E. Hill, Marjorie L. Prokosch, Amanda Morin and Christopher D. Rodeheffer examined the possibility that the consumption of artificially sweetened drinks and foods might produce unintended physiological, psychological, or behavioral changes that hinder, rather than help, consumers’ weight management goals. In doing so, they tested the impact of non-nutritive sweetener (NNS) consumption (via a diet soft drink) on food-related cognition, consumer choice, and subjective responses to sugar-sweetened snacks. In contrast to previous SuppVersity posts today's approach to the "Sweetener Conundrum" is thus a psychological, not a physiological one. One that is based on the measurement of the impact of nun-nutritive sweeteners on processes, of which we known that they will have an impact on food regulation over time. The purpose is thus to answer the all-important question whether NNS are a hazard to your weight loss / maintenance goals.

So what did the scientists do?

Now that we've successfully set the scene, let's take a look at the experimental approach Hill and her co-workers chose. As I previously hinted at, the study comprised three different experimental conditions:

• Experiment 1 -- The goal of our first experiment was to examine the impact of non-caloric sweeteners on the cognitive accessibility of food items with differing levels of caloric density.
  
  The scientists expected that that – compared to participants who consumed the sugar-sweetened or unsweetened beverage – those who consumed the beverage sweetened with NNS would have shorter response-time latencies to the names of high-calorie, but not low-calorie, food items. 
  
  What's the significance? If the hypothesis was correct this would mean that people who consume NNS are more likely to respond to high-calorie food clues. Practically speaking, they would thus be more tempted to give in and buy the a pack of candy from a street seller in New York City, when all they'd actually want to do was to pass by and catch the next taxi.
• Experiment 2 -- The goal of the second experiment was to extend the results of experiment 1 by testing the effects of NNS-sweetened beverages on people’s decision-making in a consumer choice scenario.
  
  In particular, the scientists were interested in whether NNS consumption influences the types of consumer products people choose when offered their choice of either a high-calorie food item (M&M chocolate candies) or one of two low- or zero-calorie, non-food items (a bottle of Ozarka spring water or a pack of Trident sugar-free gum).
  
  As I pointed out in the "what's the significance" paragraph of experiment 1, the scientists expected that eh participants who consumed the NNS-sweetened beverage would choose to take the high-calorie candy at a greater frequency than would those who consumed the sugar-sweetened or unsweetened drinks.
  
  What's the significance? If the hypothesis was correct and the subjects would be more likely to give in to the temptation of high-calorie candies, this would confirm that the abstract and practically irrelevant decrease in response-time latencies translates into a higher likelihood of giving in to sweet temptations.
• Experiment 3 -- The goal of our third and last experiment was to build on the results of experiment 1 and experiment 2 by examining whether consuming NNS disrupts individuals’ subjective responses to subsequently consumed sweetened foods. 
  
  As Hill et al. point out, "[m]uch research has found that NNS consumption does not influence the number of calories consumed in a subsequent meal or snack" (see Bellisle & Drewnowski, 2007 for a review). However, because consuming NNS disrupt the natural pairing of sweet taste and energy availability, consuming them may degrade the hedonic response to sucrose-sweetened food, impairing the body’s ability to regulate energy and body weight (Swithers &
  Davidson. 2005 & 2008).
  
  Thus, experiment 3 was designed to test the possibility that NNS would disrupt normal sweet perception experimentally by examining the impact of NNS-consumption on participants’ satisfaction with a subsequently-consumed, sugars-weetened snack.
  
  What's the significance? If the subjects would in fact feel less satisfied after consuming a sweet snack, when they'd been consuming non-nutritively sweetened drinks before, this would increase the chance of overeating. In other words, the one piece of chocolate that would have been enough to satisfy the chocolate cravings of someone who abstains from NNS may well trigger a "fatal" chocolate binge in NNS junkies.

The subjects of choice for this set of experiments were 116 undergraduates (75 women,
41 men). Participants’ ages ranged from 18 to 25 years (M=19.81, SD=3.27) and all received partial course credit in exchange for their participation.

No(!) difference between natural and artificial sweeteners: While you may argue that the different forms of sweeteners could have differential effects on physiological processes, the lowering of the sweetness threshold will depends - if on anything - on the degree of sweetness. Stevia would thus not be better than the (imho) falsely decried aspartame, of which I am getting tired to repeat that it is not toxic in the amounts you will find in foods and artificially sweetened beverages.

The design of the study was a 3(drink condition: Sprite vs. Sprite Zero vs. mineral water, between subjects) × 3(word type: high calorie vs. low calorie vs. non-word, within subjects) mixed factorial design. During recruitment, all participants were instructed not to eat or drink anything other than water past midnight prior to their testing session. In order to minimize unwanted influences of the subject's individual eating / drinking habits, anyone who ate or drank anything other than water less than eight hours prior to their session was excluded from all analyses (18 excluded).

All testing sessions were conducted between 8:00 and 11:00a.m. After arriving in the laboratory, participants were given a participant ID number that was linked to their testing condition. Upon being seated, participants were given an unmarked, red plastic Solo cup that contained one of three 12 ounce (355 ml) beverages: (1) sugar-sweetened (Sprite), (2) non-calorically sweetened (Sprite Zero), or (3) unsweetened (Kroger brand lemon-lime sparkling mineral water) -- The nutritive value of the test drinks is depicted in Table 1.

"I see sweet high calorie feeds, wherever I look!"

Participants (all condition-blind) were given five minutes to consume their drink while watching images from the Hubble Telescope on their computer screens. After this time had elapsed, participants were asked to complete a lexical decision task (described below). The study closed with participants being asked to respond to a series of questions about themselves (e.g., sociodemographic questions, height, weight) and about their compliance with the experimental procedure. After the experiment was complete, a hypothesis-blind research assistant used the ID numbers to match participants’ computerized data with the drink condition to which they were assigned.

"After participants finished their beverages they completed a lexical decision task to measure the cognitive accessibility of high and low-calorie foods. During this task, participants were pre sented with 28 letter strings. These letter strings, presented in random order, consisted of seven high-calorie food words (e.g., burger, cookie, pizza), 7 low-calorie food words (e.g., celery, radish, carrot), and 14 non-words (e.g., ebusun, ganeap, tigne). Each letter string flashed on the screen for 250 ms and participants had to indicate whether each letter string was a word or non-word by pressing the “z” or “m” key, respectively. The response latencies (i.e., how long it took for participants to indicate if a string of letters was a word or non-word) served as our dependent variable, with lower response latencies indicating greater cognitive accessibility. To familiarize participants with this task, before completing the experimental trials, participants completed 30 practice trials consisting of 15 neutral words and 15 non-words."

In a pre-test the scientists had made sure that all participants were aware of he high energy content and potential fattening effect of the items.

Table 2: Descriptive statistics for total number and the reaction time (in milliseconds) of words categorized correctly during a lexical decision task. Longer reaction time latencies indicate lower cognitive accessibility (Hill. 2014)

The results of the researchers 3×3 mixed-model ANOVA (a statistical analysis of the results) revealed a significant interaction between drink type and RT-category. The results of the follow-up tests indicated no significant main effect of drink type on participants’ RT to low-calorie food words. The main effect of the drink on participants’ reaction times to high-calorie food words, of which the scientists had expected that it would occur, on the other hand, was confirmed.

"Orthogonal planned comparisons revealed that participants who consumed the NNS sweetened beverage responded more quickly to the names of high calorie food items compared to those who consumed either the sugar-sweetened or unsweetened drink (p=.001, CI:−84.89,−20.11)."

What's also interesting is that there were no differences were found between the sugar-sweetened drink and those who consumed the mineral water (p=.28). The effect is thus NNS and not "sweet"-specific!

"Sweets, I see you!" Question: Will you also consume thee?

In the follow up experiment, which had the exact same baseline design and was conducted with the exact same test drinks, the participants were instructed to take the lid off of an opaque (6”×10”) green IKEA box that was located on the far right of their partitioned computer space. Inside the box were three consumer products: (a) a 12 ounce bottle of Ozarka natural spring water, (b) a pack of Trident gum (18 sticks, original flavor), and (c) an 8 ounce bag of plain chocolate M&M candies.

 "Participants were prompted by the computer to pick each product up one at a time (order was randomized via Qualtrics) and evaluate the product’s logo, packaging, and their familiarity with the product. At the end of the experiment, participants were told that they could choose one of the  products to take with them when leaving. Participants were then thanked, debriefed, and dismissed." (Hill. 2014)

After participants exited the lab, the research assistant inspected each of the boxes and made note of which product was chosen by each participant using their ID number.

Table 3: Percent of participants in each drink condition who chose a specific food option to take home. Three participants took none of the items (Sprite:n=1, Sprite Zero:n=2 | Hill. 2014)

As you can see in Table 3, both men and women displayed the same likelihood of taking the candy (p=.50) with a significant main effect of drinking the NNS beverage which increased the participants likelihood to pick the candy as their preferred take-away by 193%! Again, not difference was found between subjects who had consumed the sugar-sweetened vs. unsweetened drinks (p=.62).

A similar result was observed in the last and final experiment. After having realized that there is no sex-difference between male and female participants, the researchers conducted this last experiment, in the course of which their now exclusively female subjects were - once again! - randomly assigned to consume (1) sugar-sweetened (Sprite),  (2) non-calorically sweetened (Sprite Zero), or  (3) unsweetened (Kroger brand lemon-lime sparkling mineral water).

Table 4: Descriptive statistics for participants’ food ratings and calorie consumption by drink condition (Hill. 2014).

Afterwards they were told that were going to be evaluating how consumers evaluate food items when they are presented either in or out of their packaging. After clicking the continue button, participants were all told that they were in the ‘no packaging’ condition and that they would be evaluating a popular brand of cookies that would be brought to them in a serving bowl. At this point, a trained research assistant (all female) brought the participants the contents of a one ounce bag of mini Oreo cookies served in a disposable bowl. Participants were then instructed to sample the cookies so that they could answer some questions about them (a suspicious probe revealed that none of the subjects realized they were fooled).

Artificially sweetened beverages do not trigger overeating in healthy females

Since the participants were told to eat at least one cookie, but that they could eat as many as they liked, the scientists were able to determine that the type of drink type did not influence how good/bad participants thought that the cookies tasted (p=.51). It did yet also reveal (and that comes as a positive surprise) that the different beverages did not influence how much of the product participants consumed, either (p=.65).

What the NNS consumption did do, though, was leaving the participants significantly less satisfied with what they had eaten compared to those who consumed either the sugar sweetened or unsweetened drink. Whether that would have made them grab another Oreo, piece of chocolate or whatever only minutes after the test, however cannot be determined on the basis of this study.

While I won't change my previous recommendation, I would still like to point out that people who suffer from binge eating (disorder) may have a significantly harder time controlling their cravings, when they mess with the satisfying effects of sweets by increasing the  sweetness threshold that is required to satisfy their sweet tooth.

Bottom line: The study at hand clearly confirms that the consumption of sugar sweetened beverages will increase one's appetite for sweet(s). What it did not prove, though, is that this will necessarily increase the consumption of sweet (high calorie) foods.

In view of the fact that sticking to any diet requires a certain amount of dietary restraint and considering the fact that the researchers didn't find an immediate increase in energy consumption from sweet foods in response to the ingestion of non-nutritive sweetener, the message of the study is that using artificial sweeteners may make it harder to control your cravings. What they don't to, however, is actively trigger sugar-binges in healthy individuals; and imho that's not enough to modify my previous recommendation which was to use NNS sparingly. If you actively monitor your food consumption, they are not going to hinder weight loss or increase your propensity of gaining weight | Comment on Facebook!

References:

• Hill, Sarah E., et al. "The effect of non-caloric sweeteners on cognition, choice, and post-consumption satisfaction." Appetite (2014) | Accepted Manuscript.
• Wright, Katharine Mary. "Nonnutritive Sweetener and Weight Management: A Potential Paradox in Modern Dieting." UNF Theses and Dissertations (2014).

Sex-Differences in Cravings After Std. Meals W/ Different Macro Composition - Low Carb + Energy Meals and / or High Amounts Of Fats May Make Female Sugar Cravings Worse

When it comes to carvings, women are more susceptible to the sugar coating of a doughnut vs. steak in a salt crust.

When I saw the results of a recent study from the University of Tokushima Graduate School, I felt reminded of my last barbecue with a couple of friends and how I would have preferred another steak, when my female friends devoured the chocolate cream grimacing as if they were about to have an orgasm.

You're asking yourselves what this anecdote could possibly have to do with the latest nutrition research from Japan? Well, it confirms the main findings Zhou et al. present in their latest paper in the peer-reviewed journal Public Health Nutrition (Zhou. 2014): Men have a significantly stronger desires for salty and fatty foods, whereas women prefer sweet food after meals.

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Before we get into further details (e.g. the fact that the sweetness desire in women was stimulated by increasing fat content of the meal), let's briefly take a look at the study design, first -- The subjects were 130 residents of the Tukushima area who were assigned to two age- and BMI-matched groups according to their sex.

A randomized crossover design was used to investigate each test meal at lunchtime with a 1-week interval between testing sessions. Participants were asked to refrain from skipping meals, to refrain from drinking excessive alcohol and to maintain exercise at a consistent level before each scheduled session. During the study period, participants were randomly assigned into four groups for meals distribution. Group A and group B were administered meals following the sequence of lower to higher ED, and group C and group D were administered meals in the opposite manner. A packed test lunch was systematically provided on aspecified day for six consecutive weeks (Table 1)."

The study was designed such that the majority of daily food and energy consumed was from the test foods, according to the 2010 Dietary Reference Intakes for Japanese.

The male vs. female difference and the female sweet tooth are not completely new: Previous studies have already suggested that men are easy to satisfy with salty foods (Rolls. 1981 & 83). Havel et al. on the other hand were able to show that high fat meals reduce the 24h leptin concentration in women (Havel. 1999) and will - at a molecular level - increase the risk for sweet cravings (Ninomiya. 2001) - an energy dense high(er) carbohydrate meal has after all been shown to bring leptin levels back up (Romon. 1990). No wonder Drewnoski et al. found that obese US women tended to list predominantly sweet foods, such as doughnuts, cookies and cake, while obese men list mainly protein/fat sources (meat dishes) among their favorite foods (Drewnowski. 1992)

Six types of packed lunches were used as test meals with their basic composition and appearance remaining constant (see Table 2). As you would expect from any "truly" Asian diet, rice was the staple food, and the main dishes were sautéed beef, steamed shiitake mushrooms with mincedfish and mixed Japanese hotchpotch consisting of sweet potato, carrot, radish, dried shiitake mushrooms, bamboo shoot, lotus root and konjac.

Table 1: Randomized crossover study design of six different types of test meals* in six experimental sessions (Zhou. 2014)

A green vegetable and kelp seaweed salad as well as tomato and broccoli jelly were also served as an integral part of each meal. The test meals were varied by adding oil or by varying the volume of ingredients and the amounts (80 g or 240 g) of raw vegetable, which were consumed after cooking. The six meals were provided on each test day with varied energy and energy density (ED) as follows:

1. control meal (Control), energy 500 kcal and ED 0·8 kcal/g; 
2. high-meat/low-rice meal (Hmeat), energy 513 kcal and ED 0·7 kcal/g; 
3. low-vegetable meal (Lveg), energy 427 kcal and ED 1·0 kcal/g;
4. medium-fat/low-vegetable meal (MfatLveg), energy 520 kcal and ED 1·2 kcal/g); 
5. high-fat meal (Hfat), energy 896 kcal  and ED 1·3 kcal/g; and 
6. high-fat/low-vegetable meal (HfatLveg), energy 824 kcal and ED 71·8kcal/g

As you can see, the six meals, which differed in vegetable amounts and energy content, were primarily divided into two versions: (i) high-vegetable-content meals contained 240 g of vegetables, which included Control, Hmeat and Hfat meals; and (ii) low-vegetable-content meals contained 80 g of vegetables, which included Lveg, MfatLveg and HfatLveg meals. 

Table 2: Energy and macronutrient composition of the test meals (Zhou. 2014)

The Control, Hmeat and MfatLveg meals had low energy content with approximately 2092 kJ (500 kcal) but different nutritional composition in terms of the protein:fat: carbohydrate ratio.

Alright, let's finally get to the results - Women like sweets and low rice (carbohydrate) and high fat intake make them irresistible, no matter how much veggies they eat

The main study outcomes were the appetite for fullness, satisfaction and prospective demand, and palatability desire for savoury, sweet, salty and fatty foods ratings, the subjects rated after the individual test meals on a 100 mm visual analogue scale (VAS).

"For example, fullness and satisfaction were rated on the 100-mm lines preceded by the questions: ‘How full do you feel right now?’ and ‘How much satisfaction do you feel right now?’, and anchored on the left by ‘not at all’ andontherightby ‘very much’, respectively." (Zhou. 2014)

All participants had been familiarized with the procedure before the first tests were run. We can thus expect that they were able to accurately report their desire for sweet, salty and fatty after consuming the test meals.

Figure 1: Sweet, salty and fatty desire after test meals in men (top) and women (bottom; Zhou. 2014)

If you compare the "sweet desire" of men and women after the test meals, you will realize that the sweet desire of the female subjects was  - independent of the meals macronutrient composition - approximately 25% higher than that of their male peers.

Women are hedonic eaters and into both fat (for flavor) and sweet 

Compared to the men, the women were also much more susceptible to the palatability increase due to increased fat content (compare the graphs on the left to those on the right hand side, Figure 2).

Figure 2: Fullness and satisfaction after test meals in men (left) and women (right; Zhou. 2014).

An increase in fullness, on the other hand, was not achieved by increasing the fat content. And if you go back to the post-meal sweet desire, a high fat content (red dots) did not necessarily reduce the female desire for a sweet dessert, either. In fact, when the meal was changed to the Hfat meal with an
increased fat content by adding oil, sweetness desire was higher in women than in men from 4 h after the meal. The scientists interpret these findings as follows:

Previous studies show: The often-cited increased satiety effects of high fat meals does not exist in women. In response to high fat breakfast and lunch condition (75% fat in the hyperlipidemic vs. 75 % carbohydrate in the hyperglycemic) the 14 young women who participated in a 2003 study by Monteleone did not feel more satiated than they did after the isocaloric (=identical energy content) 75% carbohydrate (closed circles) condition - on the contrary (Monteleone. 2003)!

"Fat, as an important factor increasing palatability in a meal, enhances sensitivity to satisfaction signals by elevating leptin and insulin signalling in the central nervous system (Riedy. 1995; Williams. 2006) .The pleasurable aspects of fat consumption provide a hedonic preference for food due to the rewarding and reinforcing properties of some dietary fats (Drewnowski. 1997; Figlewicz. 2009).

The current study reflects that fat might suppress sweetness desire in a diet with vegetable content as low as 80 g, whereas in a diet with sufficient vegetable content such as 240 g, increased fat content might stimulate the redundant sweetness desire. This stimulation is probably due to initiating a vicious cycle from the increased palatability of the diet. A previous study reported that the increased fat content that promotes the sensory properties of the diet causes insulin/leptin resistance, resulting in more food consumption." (Zhou. 2014)

In other words: The high fat content annuls the beneficial effect of high vegetable intakes - at least in women. Who tend to have a higher tendency for sweet cravings, anyway - a tendency that was strengthened by high fat intakes and triggered and amplified by reduced rice intake as it was the case in the high meat + low energy diet in the study at hand.

Veggies work: One of the most important, yet by no means novel results of the study is that increasing vegetable intake in a diet is effective to enhance fullness and satisfaction regardless of gender. This is thus independent of the increased sweet desire in women with high fat + high vegetable intake.

Bottom line: Is it really just coincidence that the high meat, low energy low carb diet, that triggered the most significant carb cravings is exactly the diet those women are following who email me complaining about being unable to control their cravings - particularly their cravings for sweets? I don't think so and the scientist who highlight in their conclusion that "sweetness desire, especially for women, is also stimulated by decreasing rice [from 150 g to 100g | -33%] intake in the low-ED diet model" (Zhou. 2014) would certainly agree; and that in spite of the fact that they rightly point out that due to the restriction to just one single staple food (rice) the study would have to be repeated with "a Western diet model with bread as the staple food" to find out whether the results may be different | Comment on Facebook!

Reference: 

• Drewnowski, Adam, et al. "Food preferences in human obesity: carbohydrates versus fats." Appetite 18.3 (1992): 207-221.
• Drewnowski A (1997) Why do we like fat? J Am Diet Assoc 97, 7 Suppl., S58–S62.
• Figlewicz DP & Benoit SC (2009) Insulin, leptin, and food reward: update 2008. Am J Physiol Regul Integr Comp Physiol296,R9–R19.
• Havel, Peter J., et al. "High-fat meals reduce 24-h circulating leptin concentrations in women." Diabetes 48.2 (1999): 334-341. 
• Monteleone, Palmiero, et al. "Differential responses of circulating ghrelin to high-fat or high-carbohydrate meal in healthy women." The Journal of Clinical Endocrinology & Metabolism 88.11 (2003): 5510-5514.
• Ninomiya, Yuzo, et al. "Leptin and sweet taste." Vitamins and hormones 64 (2001): 221-248.
• Romon, M., et al. "Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake." American Journal of Physiology-Endocrinology And Metabolism 277.5 (1999): E855-E861.
• Rolls BJ, Rolls ET, Rowe EAet al. (1981) Sensory specific satiety in man.Physiol Behav27, 137–142.
• Rolls ET, Rolls BJ & Rowe EA (1983) Sensory-specific and motivation-specific satiety for the sight and taste of food and water in man.Physiol Behav30, 185–192.
• Ryan KK, Woods SC & Seeley RJ (2012) Central nervous system mechanisms linking the consumption of palatable high-fat diets to the defense of greater adiposity.Cell Metab 15, 137–149.
• Williams DL, Baskin DG & Schwartz MW (2006) Leptin regulation of the anorexic response to glucagon-like peptide-1 receptor stimulation.Diabetes55,3387–3393.
• Zhou, B., Yamanaka-Okumura, H., Adachi, C., Kawakami, Y., Katayama, T., & Takeda, E. (2014). High-fat diet-related stimulation of sweetness desire is greater in women than in men despite high vegetable intake. Public health nutrition, 1-10.

They Dictate What You Like, They Dictate What You Crave and They May Even Determine Whether You're Lean or Fat: The Bacteria in the Gut - The Latest Evidence Reviewed

The alien inside - billions of bacteria in your gut interact with your central nervous system and take command over your metabolism and - probably - even about what you want to put into your mouth.

Wouldn't it be great if it was not your lack of willpower and your unhealthy food choices that were to blame for the potbelly you're carrying around? Wouldn't it be awesome if you could blame your misery on someone else? And wouldn't it be best if that someone was a dirty little microbe in your gut? Someone who cannot fight back, when you chose him as a scapegoat? That would be great, right?

Well, in today's SuppVersity Article we're going to take a look at a bunch of studies and hypothesis that may actually allow you to find a new excuse for your inability to lose weight. But beware! While I wouldn't say that researchers who favor the "evolutionary conflict between host and microbes" theory as an alternative explanation for the ever-increasing obesity rates are totally off. What I will say, however, is that this is at best a contributing, maybe even just a corollary factor in the etiology of the obesity epidemic.

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We know for quite some time that individual members of the microbiota, and consortia of those microbes are highly dependent on the nutrient composition of the diet.

• Prevotella grows best on carbohydrates; dietary fiber provides a competitive advantage to Bifidobacteria (González‐Rodríguez. 2013)
• Bacteroidetes has a substrate preference for certain fats (Wu. 2011)

Scientists have also found some specialist microbes, e.g. mucin degrading bacteria such  as Akkermansia mucinophila. They thrive on secreted carbohydrates provided by host cells. Other butyrate producing microbes, e.g. Roseburiaspp., fare better when they are delivered polysaccharide growth substrates in the diet. Specialist microbes that digest seaweed have been isolated from humans in Japan (Hehemann. 2010). African children raised on sorghum have unique microbes that digest cellulose (De Filippo. 2010). Many other examples exist (Fava. 2012).

We have tons of associations, but little experimental evidence: All this does yet not mean that the specialized gut microbiome will also affect the dietary intake of the host. You could after all argue that you could get rid of Prevotella by simply cutting out all carbs from your diet, but scientists believe that the specialization works both ways.

There is circumstantial evidence for a connection between cravings and the composition of gut microbiota. Individuals who are “chocolate desiring” have different microbial metabolites in their urine than “chocolate indifferent” individuals, despite eating identical diets (Rezzi. 2007).

Figure 1: A study by Rezzi et al. showed that chocolate cravers have a different microbiome than their peers (Rezzi. 2007)

In spite of these intriguing results and a plethora of evidence for mood and central nervous system effects of certain bacteria in rodents, the definite evidence of a causal relationship between gut microbes A, B & C and certain food preferences, let alone "addictions" is still missing.

It's not as if there was no evidence, it's just not really compelling (yet?)

An area where the mechanisms appear to be more evident is the effect of certain bacteria on the expression of certain molecular receptors in the gut. Germ-free mice for example have altered taste receptors for fat on their tongues and in their intestine compared to mice with a normal microbiome (Duca. 2012). Since an increase in fat receptors is associated with an increased preference and intake for fatty foods and energy, an over-expression of these receptors could certainly be involved in the etiology of obesity.

Both, low dose penicillin at weaning (blue) and at birth (red) lead to significant obesity in male pups later in life (Cox. 2014).

Latest research says: Disruption of gut bacteria early in life can lead to obesity in adulthood! Certain microbes found in the gut may protect against obesity and diabetes. A study published by Cell Press August 14th in the journal Cell reveals that these microbes shape their hosts' metabolism very early in life and that disrupting them with short-term exposure to antibiotics during infancy can cause metabolic changes that appear to increase the risk of obesity in adulthood.

These findings in mice are helping researchers identify which gut bacteria are crucial to metabolic health. Such information could be used to help restore levels of those helpful microbes after an infant has received life-saving antibiotics, thereby promoting healthy metabolism in adulthood.

In conjunction with other scientific evidences, such as the increased intestinal expression of cannabinoid and opioid receptors in mouse and rat intestines in response to the oral supplementation of L. acidophilus NCFM in rats and similar effects in human epithelial cell culture (Rousseaux. 2006), the Duca study suggests that the composition of microbes in our guts could in fact actively alter our food preferences by modulating the receptor expression or transduction (Collins. 2012).

Is a "gut dysbiosis" the reason we are fat?

The idea that not having the "right" bacterial make-up could be at the heart of the obesity epidemic has recently received significant scientific attention. Backhed and colleagues showed that mice genetically predisposed to obesity remained lean when they were raised without microbiota (Bäckhed. 2004).

Figure 2: Germ-free mice stayed lean, in spite of the fact that they were genetically predisposed to become obese and irrespective of their increased food intake (Bäckhed. 2004). When they were inoculated with the microbiota from regular obese mice (CONV-D), however, they became just as obese as their conventional peers (CONV-R)

When the mice were "infected" with fecal pellets from a conventionally raised obese mice, they became obese again. That this could happen in humans as well is supported by data from Ridaura et al. (2013) who observed that the inoculation of germfree mice with microbiota from an obese human produced similar results.

Let's put everything together, now!

As you can see in the graphical illustration in Figure 3, the taste receptor interactions are not the only scientifically proven changes. There are also well-known endotoxin induced effects on mood and anxiety (Amaral. 2008; Chiu. 2013) of which Hill et al. have shown (albeit in a different context) that it will affect food cravings (Hill. 1991).

Beware! If the scientists are right, the same probiotics that are good for people on a mixed diet may be bad for those who consume a low carb or ketogenic diet. I would thus be very reluctant to make any form of one-size-fits it all supplement recommendation! If there is one take home message from what we already know, it's that, in the long run, unbalanced diets (low-to-no whatever) will obviously put you at greater risk of developing a highly specialized obesity-promoting gut microbiome.

Figure 3: Like microscopic puppetmasters, microbes may control the eating behavior of hosts through a number of potential mechanisms including microbial manipulation of reward pathways, production of toxins that alter mood (shown in pink, diffusing from a microbe), changes to receptors including taste receptors, and hijacking of neurotransmission via the vagus nerve (gray), which is the main neural axis between the gut and the brain (Alcock. 2014)

Now Alcock et al. who created this illustration speculate that the weight loss and inhibition of weight gain we've seen in trials using probiotic yogurts (Kadooka. 2010; Mozaffarian. 2011) could be mediated, at least in parts, by microbial interactions with the vagus nerve:

If microbial control is mediated through the vagus nerve, then microbial signals should interfere to some extent with the physiological regulation coordinated by the vagus nerve. [...] We predict that people experiencing cravings should have lower vagal tone. Furthermore, it is possible to block or sever the vagus, which we predict would subdue microbial signaling via the vagus nerve, and thereby alter food preferences. This would be consistent with studies showing that blocking the vagus nerve can lead to weight loss." (Alcock. 2014)

In conjunction with the aforementioned effects and the influence of population size and composition on cravings and high fat, high carbohydrate preferences foods Alcock et al. believe to have enough evidence for the existence of what they call an "evolutionary conflict between the host and microbiota" which may lead to cravings and cognitive conflict with regard to food choice.

Will Engineered Super-Bacteria Help Even Gluttons to Stay Lean? Scientists "Produce" Anti-Obesity Bacteria to be Administered in the Water | more

Personally I don't consider the evidence convincing enough to assume that the suppression oo modification of microbial signals from the gut alone will fix what is currently deemed a problem of self-control and bad food choices | What's your take? Comment on Facebook!

I do not doubt though that "acquired tastes" may at least be reinforced by corresponding microbial selection in the gut. Resetting the microbial make-up and/or modifying it via pre- and probiotic foods and supplements is thus unquestionable an interesting, yet still not fully understood strategy to complement lifestyle intervention that focus on diet and exercise.

And let's not forget: Both diet and exercise have been shown to have a major impact on the gut microbiome, as well (Gotthardt. 2014; Hold. 2014)!

References:

• Alcock, Joe, Carlo C. Maley, and C. Aktipis. "Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms." BioEssays (2014).
• Amaral, F. A., et al. "Commensal microbiota is fundamental for the development of inflammatory pain." Proceedings of the National Academy of Sciences 105.6 (2008): 2193-2197.
• Bäckhed, Fredrik, et al. "The gut microbiota as an environmental factor that regulates fat storage." Proceedings of the National Academy of Sciences of the United States of America 101.44 (2004): 15718-15723. 
• Chiu, Isaac M., et al. "Bacteria activate sensory neurons that modulate pain and inflammation." Nature (2013).
• Collins, Stephen M., Michael Surette, and Premysl Bercik. "The interplay between the intestinal microbiota and the brain." Nature Reviews Microbiology 10.11 (2012): 735-742.
• Cox et al. "Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting Metabolic Consequences." Cell 158 (2014):705–721.
• De Filippo, Carlotta, et al. "Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa." Proceedings of the National Academy of Sciences 107.33 (2010): 14691-14696.
• Duca, Frank A., et al. "Increased oral detection, but decreased intestinal signaling for fats in mice lacking gut microbiota." PloS one 7.6 (2012): e39748. 
• Fava,Francesca, et al. "The type and quantity of dietary fat and carbohydrate alter faecal microbiome and short-chain fatty acid excretion in a metabolic syndrome ‘at-risk’population." International Journal of Obesity 37.2 (2012): 216-223.
• González‐Rodríguez, Irene, et al. "Factors involved in the colonization and survival of bifidobacteria in the gastrointestinal tract." FEMS microbiology letters 340.1 (2013): 1-10.
• Gotthardt, J. D., et al. "Exercise Promotes Enhanced Gut Microbial Diversity Compared to Sedentary Counterparts." International Journal of Exercise Science: Conference Proceedings. Vol. 9. No. 2. 2014. 
• Hehemann, Jan-Hendrik, et al. "Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota." Nature 464.7290 (2010): 908-912.
• Hill, Andrew J., Claire FL Weaver, and John E. Blundell. "Food craving, dietary restraint and mood." Appetite 17.3 (1991): 187-197. 
• Hold, Georgina L. "The gut microbiota, dietary extremes and exercise." Gut (2014): gutjnl-2014.
• Kadooka, Y., et al. "Regulation of abdominal adiposity by probiotics (Lactobacillus gasseri SBT2055) in adults with obese tendencies in a randomized controlled trial." European Journal of Clinical Nutrition 64.6 (2010): 636-643.
• Miras, Alexander D., and Carel W. le Roux. "Mechanisms underlying weight loss after bariatric surgery." Nature Reviews Gastroenterology and Hepatology 10.10 (2013): 575-584.
• Mozaffarian, Dariush, et al. "Changes in diet and lifestyle and long-term weight gain in women and men." New England Journal of Medicine 364.25 (2011): 2392-2404.
• Rezzi, Serge, et al. "Human metabolic phenotypes link directly to specific dietary preferences in healthy individuals." Journal of proteome research 6.11 (2007): 4469-4477.
• Ridaura, Vanessa K., et al. "Gut microbiota from twins discordant for obesity modulate metabolism in mice." Science 341.6150 (2013): 1241214.
• Rousseaux, Christel, et al. "Lactobacillus acidophilus modulates intestinal pain and induces opioid and cannabinoid receptors." Nature medicine 13.1 (2006): 35-37. 
• Wu, Gary D., et al. "Linking long-term dietary patterns with gut microbial enterotypes." Science 334.6052 (2011): 105-108.

Practical Implications of Recent Studies: Sour & Bitter Curb Cravings for Sweet & Salty | 30min 3x / Week Min. Training | Masturbation + Abstinence Boost Testosterone by ~50%

The "Curb the cravings w/ sour and bitter foods"-implication is just one out of three science-based hypothesis on potential practical implications of recent studies.

This could be the first part of a new SuppVersity article series. Not one that's published on a regular, like weekly, basis. Rather one that will appear from time to time - out of the blue, or the depth of my forehead - to cast a spotlight on potential applications of recent scientific findings.

I can already tell you that not all of them will eventually work - that's how hypothesis work: You formulate them based on the existing evidence, only to realize that you were completely missing the boat, when you argued that eating sour and bitter foods will help you shut down your junk food cravings... which reminds me: Let's not lose additional time and get right to implication numero uno which is, ...

• Implication 1: If you are always ravenous, eat bitter or sour to stop the cravings -- As with all the tips in this first installment of what could become a regular if you signal me that you like the idea of hypothesizing about potential practical applications of the results of recent studies, you got to be careful about the real world effects of the "sour" and "bitter" taste ligand induced production of the "satiety hormone" cholecystokinin (CCK) researchers from the Nagahama Institute of Bio-Science and Technology in Japan observed in isolated gut cells (Miyata. 2014).
  
  

  

  Scheme of the regional gustatory preferences nested within the 10,000 taste buds distributed on the human tongue (Slavkin. 1999)

  In view of the fact that neither sucrose (sweet taste) nor NaCl (salty) or MSG (umami) had similar effects it does not appear totally unlikely that this tip will actually work... I mean, sweet, salty and umami? That's exactly the "taste" of the SAD diet - the same diet that has spread the obesity epidemic right from its US epicenter all around the world over the past decades.
  
  And before I forget to mention it: There are "tastebuds" all over your body. The tongue is just one of them | learn more.

• Implication 2: You don't have to move mountains, but 30 minutes x three times a week is the minimal volume x frequency prescription to see significant health benefits from structured physical activity aka "exercise" -- To come to this conclusion I did not even have to come up with extra hypotheses. Actually Heather J. A. Foulds and colleagues, who have recently reviewed the existing literature to elucidate "the relationship between exercise volume and intensity and health benefits" and the results,... well, the results are actually what the tip already said: 

  "In healthy active individuals, a physical activity program of at least 30 min in duration for three sessions/per week is associated with consistent improvements in health status." (Foulds. 2014).

   The scientists also found that upping the intensity from brisk waling to jogging is associated with an additional increase in cardiovascular health benefits. If that's exactly the best thing for your knees is anyone's guess, though. 

• Implication 3: If you believe in the power of testosterone and want to perform your best at a meet next week, masturbate today! -- According to researchers from the Department of Life Science, at the Hangzhou Normal College in China, the serum testosterone concentrations of their 28 volunteers changed significantly in response to ejaculation at the end of a period of abstinence. While, the fluctuations of testosterone levels from the 2nd to 5th day of abstinence were minimal, a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01) on day 7 (Jiang. 2003). 
  
  The scientists are careful to point out that "[e]jaculation is the precondition and beginning of the special periodic serum testosterone level variations", though. In other words: Years of abstinence are not going to have a similar effect, as a 7-14 day rhythm would have... what? You willingly pass on maxing out your testosterone levels by cyclic abstinence? Well, I can understand that ;-)

Table 1: Methodological issues in sexuality research with testosterone and other androgens in humans, and suggested practices for addressing them (van Anders. 2014) - just in case you plan to test, whether implication #3 works ;-)

Mini-Summary: Alright, the things you learned today are "potential",... well, the increase in testosterone mentioned in the last of three tips is going to be very real, but the implications, i.e. potential performance increases probably not. The benefits of regular activity, even if it's only 30 minutes thrice a day, on the other hand, is beyond doubt.

Unfortunately, that's something of which I am not sure that you can say it about the satiating effects of sour and bitter foods. Ok, you probably won't overeat on bitter green tea leaves, but it still requires more self-control than many people apparently have, not to put away the green tea leaves you may be snacking on in front of your TV and replace them with a mix of chocolate, and chips: sweet, salty, and 100% non-satiating - just the way we like it.

References:

• Foulds, Heather JA, et al. "Exercise volume and intensity: a dose–response relationship with health benefits." European Journal of Applied Physiology (2014): 1-9.
• Jiang, Ming, et al. "A research on the relationship between ejaculation and serum testosterone level in men." Journal of Zhejiang University SCIENCE A 4.2 (2003): 236-240.
• Miyata, Mutsuki, et al. "Effect of five taste ligands on the release of CCK from an enteroendocrinecell line, STC-1." Biomedical Research 35.2 (2014): 171-176.
• Slavkin, Harold C. "Toward'molecular gastronomy,'or what's in a taste?." Journal of the American Dental Association 130 (1999): 1497-1500. 
• van Anders, Sari M., Katherine L. Goldey, and Sarah N. Bell. "Measurement of testosterone in human sexuality research: Methodological considerations." Archives of sexual behavior 43.2 (2014): 231-250.

L-Tryptophan is Reduced While Dieting - Does This Make the Essential Amino Acid a Key to Succesfull Weight Loss?

Trp and it's metabolite 5-HTP may be particularly useful for female sugar cravings and binges.

Can l-tryptophan help you lose body fat? If you look at the results of the latest study from the University for Health Sciences, Medical Informatics and Technology it would seem that the answer to this question may be "Possibly, yes, but..." Before we come to the implications I would yet like to take a closer look at said study which shows that a lack of tryptophan (Trp) during diets does not just affect the biosynthesis of serotonin, but may also be associated with increased susceptibility for mood disturbances and carbohydrate craving. Accordingly, "strategies to supplement Trp while dieting could be highly useful in treating uncontrolled weight gain or in preventing neuropsychiatric symptoms" (Strasser. 2014).

Honestly, fasting and eating / skipping breakfast may be more promising weight loss tools

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Breakfast & Glucose Metab.

Breaking the Fast, Cardio & the Brain

Does the Break- Fast-Myth Break?

Fasting = Muscle- Loss - Always?

As Strasser et al. point out, both overweight and obesity go hand in hand with significant increases in low-grade inflammation. The latter is not just the reason that obesity increases the risk of cardiovascular disease, though. Recent evidence suggests that it is also associated with errors in the kynurenine (Kyn) pathway, in which tryptophan is broken down to kynurenine which in turn has been associated with increased risk of depressive symptoms, cognitive deficits in schizophrenia, Alzheimer's and, as mentioned before, cardiovascular disease. Weight loss, on the other hand,

"[...] has been shown to improve or prevent many of the aforementioned conditions. Bariatric surgical intervention in patients with adiposity was found not to improve tryptophan breakdown rates and other signs of immune activation and inflammation [4], whereas caloric restriction is known to be a strong activator of protective metabolic pathways, thereby leading to lower blood pressure, improved blood lipids, and reduced inflammatory markers, including CRP [9]. Still, little is known about the effects of an extreme short-term hypocaloric diet on Trp metabolism and changes in inflammatory biomarkers" (Strasser. 2014).

The study Barbara Strasser, Ken Berger and Dietmar Fuchs conducted was thus designed to assess the effect of a 2-week caloric restriction weight loss diet on Trp breakdown, leptin, and inflammatory biomarkers in over weight adults.

Taking tons of BCAAs can deplete your brain Trp and serotonin and leave you tired and depressed.

Beware of your beloved BCAAs,  Trp competes with the other large neutral amino acids (LNAA), namely valine, leucine, isoleucine, Tyr, and Phe for transport across the blood–brain barrier. In fact, scientists use large boluses of BCAAs to practically deplete tryptophan and thus reduce serotonin (Fernstrom. 2005). If you want to learn more about this unwanted side effects of BCAA, I'd suggest you take another look at my article "The Neurotransmitter Depleting Effects of Branched Chain Amino Acids (BCAAs) and Their Potential Ergolytic, Anxiogenic & Depressive Downstream Effects" | read more.

The scientists randomized 27 overweight and 11 obese participants (22 men and 16 women, mean age 52.8 ± 9.1 years) from the health center Lanserhof, Innsbruck–Lans, into two diet groups:

• a very low kcal diet group (VLCD; Ø 600 kcal/ day) and 
• a low kcal diet group (LCD; Ø 1,200 kcal/day). 

Only healthy subjects with BMI [25 kg/m²] between the ages of 35 and 70 years were accepted for the study. A physician performed physical examinations on all subjects before the study. Subjects were excluded if they consume any anti-inflammatory drugs (e.g., ibuprofen or aspirin) or supplements (such as antioxidants or fish-oil capsules). None from either group was involved in regular training programs.

Figure 1: Changes in body composition pre- vs. post (Strasser. 2015).

As the measurements of body composition, which were just like the energy intake and biologic markers conducted in all subjects before and after the 2-week energy restriction intervention period, indicate, both diets lead to significant reductions in body mass - and that almost exclusively in form of body fat.

Table 1: Biologic markers before and after a 2-week very low kcal diet (VLCD) or low kcal die (LCD) in 38 overweight subjects (mean ± SD)

"Data for biologic markers are shown in Table [1]. Fasting blood glucose declined significantly (P < 0.05) in the LCD group with no significant changes in insulin sensitivity in both groups after 2 weeks of caloric restriction. Weight loss diet lowered leptin levels in both groups, although not reaching the level of significance. Inflammatory biomarkers were not significantly altered during the trial, although there was a tendency toward an increase in IL-6 and TNF-a in the LCD group" (Strasser. 2015).

In contrast to what the researchers expected, both the Trp and Kyn concentrations decreased significantly by 21 and 16 % for VLCD and by 15 and 17 % for the LCD group, respectively, with no significant difference between groups. Practically speaking, this means that the ratio of Kyn/Trp concentrations did not change significantly in both groups.

Adding 900mg 5-HTP to the diet of obese women helps them to reduce their energy intake significantly (Cangiano. 1992).

5-HTP the better choice? While it makes sense to keep an eye on the Trp:LNAA ratio in your diet, it is questionable, whether supplementing with Trp on top of a Trp-sufficient diet will have significant beneficial effects. In this respect, 5-hydroxytryptophan aka 5-HTP a direct serotonin precursor appears to be the more promising supplement. Taken in dosages of 400-1,000mg/day it has been shown to (a) reduce food intake (up to 18% more than placebo in a 1989 study w/ obese women | Ceci. 1989), (b) increase weight loss in 12-week study with obese women (Cangiano. 1992) and (c) reduced the food and specifically carbohydrate intake in both male and female type II diabetics (Cangiano. 1998).

A significant reduction in Phe concentrations was only seen after VLCD. Neopterin and Tyr levels remained unchanged during the trial. Which leaves us with only one significant finding:

"Trp concentrations decreased significantly with a caloric restriction weight loss diet, and lowest Trp concentrations were observed in the group of individuals with the lowest calorie intake." (Strasser. 2015)

This reduction in Trp levels may well induce a disturbance in the biosynthesis of neurotransmitter 5-hydroxytryptamine (5-HT | Anderson. 1990), and appears to be associated with an increased susceptibility for depression (Widnet. 2002; Raison. 2009). Strasser et al. highlight:

Figure 2: The consumption of tryptophan-free amino acid supplements leads to highly significant increases in hunger ratings in healthy female subjects (Rieber. 2010).

"Because Trp is precursor in various biochemical pathways, e.g., it is hydroxylated by tryptophan-5-hydroxylase (T5H) into the intermediate product 5-hydroxy-tryptophan, which by decarboxylation is further converted to neurotransmitter 5-HT (serotonin), and because substrate saturation of T5H is only about 50 % (Dantzer. 2011), changes in plasma Trp levels may have an immediate impact on brain serotonin levels" (Strasser. 2014).

Experiments in which Trp was acutely depleted (in many studies by administering BCAAs | see red boy) support this assumption. Young et al. (2013), for example, confirmed that the acute depletion of tryptophan will lead to low serotonin and subsequently lower mood and increased aggression, although results vary somewhat between studies with similar participants.

Figure 3: Correlations between changes in tryp:LNAA ratio and appetite ratings (Gendall. 2000).

For the link to obesity, though, the correlation (r-values in Figure 3) between high Trp:LNAA (BCAAs, tyrosine, phenlylanine) and a reduction carbohydrate cravings, general hunger and binge eating is yet way more important - and that specifically for women, who appear more vulnerable than men both to the diet-induced reductions in Trp and to its consequences for brain serotonin function (Anderson. 1990).

Ah, and in case you are asking yourself why carbohydrate / sugar binges are a common consequence of low tryptophane:LNAA ratios, it's important to know that increases in glucose and insulin in response to high carbohydrate meals will trigger an increase in brain tryptophan and serotonin synthesis (Benton. 2002). This is why the effects of low tryptophan or high LNAA (BCAA, tyrosine, phenylalanine) levels are more pronounced if you avoid dietary carbohydrates.

There is evidence of direct effects of serotonine on metabolic rate, but there is no evidence that the administration of Trp will induce similar increases in fatty acid oxidation and thermogenesis as serotonin (Le Feuvre. 1991; Cui. 1993). It does therefore remain speculative whether the use of tryptophan supplements will have beneficial effects on the success of your next diet that go beyond an increased ability to stick to your predetermined caloric deficit due to reduced hunger and (CHO) cravings. Furthermore it's not 100% clear whether taking 5-HTP which is significantly closer to serotonin would have different and/or more pronounced beneficial effects compared to its precursor Trp.

This raises the question: Does supplementation help? It's one thing to observe correlations, it's another thing to have scientific evidence from controlled trials which support a causative link between higher tryptophan intakes and/or supplementation and increased adherence to calorically restricted diets and/or reduced cravings and binges.

Let's take the study by Rieber et al. (2010 | Figure 2), for example, in their study a tryptophan-free amino acid supplement like the ones people sell as muscle builders lead to significant increases in hunger scores in healthy young women. Only recently, scientists from the University of Barcelona were able to show that chronic treatment with a tryptophan-rich protein hydrolysate improves emotional processing, mental energy levels and reaction time in middle-aged women. A result that suggests that chronic vs. acute treatments may have different effects, as well.

Direct evidence that tryptophan will also affect the reduction in energy expenditure, when dieting is yet not available from human trials. As of now, it's thus the reduction in appetite and cravings that is furthermore particularly pronounced in women that may considered among the scientifically warranted benefits of tryptophan supplementation and the avoidance of tryptophan depleting Trp-free amino acid supplements containing BCAAs, phenylalanine and tyrosine | Comment on Facebook!

References:

• Anderson, I. M., et al. "Dieting reduces plasma tryptophan and alters brain 5-HT function in women." Psychological medicine 20.04 (1990): 785-791. 
• Benton, David. "Carbohydrate ingestion, blood glucose and mood." Neuroscience & Biobehavioral Reviews 26.3 (2002): 293-308.
• Cangiano, Carlo, et al. "Eating behavior and adherence to dietary prescriptions in obese adult subjects treated with 5-hydroxytryptophan." The American journal of clinical nutrition 56.5 (1992): 863-867.
• Cangiano, Carlos, et al. "Effects of oral 5-hydroxy-tryptophan on energy intake and macronutrient selection in non-insulin dependent diabetic patients." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 22.7 (1998): 648-654.
• Ceci, F., et al. "The effects of oral 5-hydroxytryptophan administration on feeding behavior in obese adult female subjects." Journal of neural transmission 76.2 (1989): 109-117.
• Cui, Y., T. F. Lee, and L. C. H. Wang. "Thermoregulatory responses following injection of 5-hydroxytryptamine into the septohippocampal complex in rats." Pharmacology Biochemistry and Behavior 45.4 (1993): 935-939.
• Dantzer, Robert, et al. "Inflammation-associated depression: from serotonin to kynurenine." Psychoneuroendocrinology 36.3 (2011): 426-436. 
• Fernstrom, John D. "Branched-chain amino acids and brain function." The Journal of nutrition 135.6 (2005): 1539S-1546S.
• Gendall, Kelly A., and Peter R. Joyce. "Meal-induced changes in tryptophan: LNAA ratio: effects on craving and binge eating." Eating behaviors 1.1 (2000): 53-62. 
• Le Feuvre, R. A., L. Aisenthal, and N. J. Rothwell. "Involvement of corticotrophin releasing factor (CRF) in the thermogenic and anorexic actions of serotonin (5-HT) and related compounds." Brain research 555.2 (1991): 245-250.
• Nieuwenhuizen, Arie G., et al. "Acute effects of breakfasts containing α-lactalbumin, or gelatin with or without added tryptophan, on hunger,‘satiety’hormones and amino acid profiles." British journal of nutrition 101.12 (2009): 1859-1866.
• Raison, Charles L., et al. "CSF concentrations of brain tryptophan and kynurenines during immune stimulation with IFN-α: relationship to CNS immune responses and depression." Molecular psychiatry 15.4 (2009): 393-403.
• Rieber, N., et al. "Acute tryptophan depletion increases experimental nausea but also induces hunger in healthy female subjects." Neurogastroenterology & Motility 22.7 (2010): 752-e220.
• Strasser, Barbara, Ken Berger, and Dietmar Fuchs. "Effects of a caloric restriction weight loss diet on tryptophan metabolism and inflammatory biomarkers in overweight adults." European journal of nutrition (2014): 1-7.
• Widner, Bernhard, et al. "Neopterin production, tryptophan degradation, and mental depression—What is the link?." Brain, behavior, and immunity 16.5 (2002): 590-595.
• Young, Simon N. "The effect of raising and lowering tryptophan levels on human mood and social behaviour." Philosophical Transactions of the Royal Society B: Biological Sciences 368.1615 (2013): 20110375.