Tuesday, February 10, 2015

Fat is the sixth taste

The role of the sense of taste is to act as gatekeeper of ingestion, if a potential food is deemed suitable for consumption it may be swallowed, if not rejected.  To guide the decision making we have five taste qualities: sweet, sour, salty, bitter and umami.  Sweet, salty and umami are all appetitive and signal the food contains essential nutrient, while excessive sour and bitter signal aversion and potential harm. 

Over the past few years there has been considerable attention given to fat as an additional taste; it seems logical given that we have taste responses to the breakdown products of carbohydrate (sugars) that elicit sweet, and protein (amino acid) that elicit umami.

For fat to be considered a taste a chain of events must take place.  There must be a class of stimuli (fats or the breakdown products fatty acids) that activate receptors on taste cells that are specific to the stimuli.  A signal must be sent from the taste cell to taste processing regions of the brain.  The signal that is decoded as a perception must be independent of the other tastes (not a combination of sweet and salt or any other possible combinations).

The first evidence of a fat taste came out of a rat model in 1998, with Dr Timothy Gilbertson from Utah University showing a taste response to fatty acids.  Professor Richard Mattes from Purdue showed similar receptors may occur in humans when he looked at sham feeding butter or non-fat butter substitute in humans, and seeing that butter caused an increase in blood triglycerides.  The implication being that the fatty acids were activating a taste receptor system and preparing the body for fat digestion. 

The concentrations of fatty acid required to activate fat taste is very low, and in the range found in common fatty foods.  In addition, we also have lingual lipase that can cleave fatty acids from triacylglycerols, albeit with low activity.  But taken together human limits of detection for fatty acids are well within the range we find in common foods.

Various researchers have identified fatty acid receptors on taste cells with the most likely candidates for fat taste being CD36 and GPR120.  Further evidence supporting fat taste was the discovery of fat sensitive neurons in taste processing region of the brain.  Finally, using our taste methodology we have established perceptual independence from the other tastes at detection threshold level.

We started our research in 2007 and published our first paper in 2010 showing a link between fat taste and BMI, with subjects who were insensitive to fat having a higher BMI.  Since then we have published papers on method development, reliability of fat taste measures, links with overweight and obesity, links with gastrointestinal tract sensing of fat, and mechanisms that link fat taste with overconsumption of fatty foods.

The one characteristic of fat taste that is different from the other 5 tastes is a conscious quality.  For example, we place sucrose on our tongue and experience sweetness, or NaCl on our tongue and experience saltiness.  For fat taste we present 3 solutions, one of which contains a fatty acid.  The task is to identify which solution contains the fatty acid.   If the subject is incorrect the concentration of fatty acid is increased and the test rerun. This continues until the correct solution is identified multiple times.  Participants can correctly identify the fatty acid solution but cannot provide an adjective that describes any taste; they know it is different but cannot articulate why.

Questions will remain. Does no taste quality exclude fat from being classified as a taste?  Or is there a piece of information that would exclude fat from being a taste?  However, with the advances in scientific techniques, our growing understanding of the taste system and its role as the first part of the alimentary canal, emerging evidence for Kokumi and other non-traditional tastes on the horizon, it may be time to broaden the scope of how we define taste.




Saturday, March 30, 2013

Bitterness and Supertasting

Excessive bitterness turns people off consuming those foods. For example, if I eat a food and experience excessive or lingering bitterness from it, I am unlikely to consume the food again. To some people that statement may appear illogical because there are many excessively bitter foods common in the food supply; think about beer or coffee.  An important factor in this discussion is individual differences in perception and what I experience as excessively bitter, a second person may experience little to no bitterness.  In such a situation I reject the food, while the other person finds the food perfectly acceptable. Part of the diversity is due to complex biology underpinning bitter taste – we have at least 25 receptors for bitter taste, some receptors are responsive to multiple compounds, others only one or two compounds. 
Individual differences are the norm, we all have our own flavour worlds and bitter taste is particularly variable among the population. One concept common in discussions about bitterness and individual variation is the ‘supertaster’. The term is applied to a person who is sensitive, or experiences extreme bitterness from the compounds PROP (n-6-propylthiouracil) or PTC (Phenylthiocarbamide); both of these compounds activate the same narrowly tuned bitter taste receptor (meaning only a few compounds activate the receptor).  Some studies have shown that supertasters are more sensitive generally to bitterness of foods, meaning they experience a higher intensity of bitterness not just to PROP or PTC, but all bitterness.  Some studies suggest supertasters are more sensitive to all sensory stimuli.  Operationally this is not true, the term supertaster merely means an individual is more sensitive to a specific bitter compound, and may mean no more than that.  When an individual is generally more sensitive to food chemicals the heightened sensitivity to PROP / PTC may be a defacto marker of increased papillae. Given the thought that more papillae means more taste receptors, and the more receptors the greater the taste signal from the papillae. 
In the same paradigm, people who cannot taste bitterness in PROP / PTC are termed ‘non-tasters’.  This is not because they have no papillae, but because the bitter taste receptor has a minor variation in sequence compared to the receptor in supertasters.  When researchers have looked at supertasters and non-tasters as groups, some differences in food consumption are apparent in some studies – for example supertasters find broccoli and alcohol bitter and consume less of them than non tasters; other studies find no differences in consumption between the groups.
The relevance of sensitivity to PROP / PTC to food consumption is debatable because of the large individual variation to bitterness – just because I am sensitive to PROP or PTC does not mean I am sensitive to the bitterness of caffeine or myriad other bitter chemicals in the food supply. You commonly have the situation where an individual may not eat grapefruit because they find it too bitter, but have no problem consuming black unsweetened coffee. Some others may find both or neither bitter.  It can be confusing, but that is a function of the complex biology and perceptual processes involved.   
Dr John Hayes and I recently published a paper reconceptualising the supertaster terminology (1).

REFERENCE

Friday, February 15, 2013

Food Quality. What is it?

In terms of how we think about a food, the quality aspect is a perceptual process, Food Quality Perception
Food is described as any solid material that is eaten, or taken into the body for nourishment. It includes all unprocessed, semi-processed, or processed items which are intended for use as food or drinks including any ingredients incorporated into food or drink, and any substances that come into contact with food during production, processing or treatment.
Quality is a theoretical construct, a thought, idea, pattern or notion. It is not a physical entity with a fixed time or position. Quality can be defined in many ways and from many different perspectives. In food science, quality concerns a products ‘fitness for consumption’. A product is considered quality, if it satisfies all the needs and requirements relating to characteristics of food, as determined by the producer, manufacturer or consumer.
Perception is the process in which information is selected, organised and interpreted through input from our sensory systems.  Perception is shaped by cognitive processes, understandings, and experiences.  Perception is individual and influenced by memories, personality, mood, knowledge and expectations.
Quality at the retail level is based on how quickly a product disappears from the shelf, and is based on consumer demand. Whilst this may be considered a good measure of food quality, it is not always the most purchased item that is the best quality. Consider the popularity of white bread which is mass produced and sold, yet its quality merits probably lie with its versatility (can be used for toast, sandwiches) and price (it’s cheap). Most people would argue that home-baked or freshly baked breads from smaller outlets are higher quality, but at the same time are not suitable for all occasions. The quality-to-price ratio is partially responsible for differences between market performance and true quality.
What we see as quality is subjective, foods are considered quality if they meet all our desires and requirements. Personal preferences for food products based on these requirements occur as we take in and interpret information surrounding a product. We assess determinants of quality based on personal needs, knowledge, beliefs and prior experiences. Quality perception is evaluated through cues prior to purchase; after consumption quality can be re-assessed by experience. 
We use both sensory and non-sensory dimensions such as convenience and health to form quality perceptions. Information regarding food products can be evaluated both prior to purchase by touching, smelling, inspecting foods or studying labels, health claims and brands, as well as after preparation and consumption by sensations and other postingestional outcomes or convenience dimensions experienced during preparation.
Attributes of specific foods are considered desirable for different occasions, at different times and as our knowledge and exposure to food increases so does our perception of quality. Food which is chosen for a picnic would not necessarily be served at a high class restaurant, yet both could be considered quality for each occasion. Similarly food which needs to be eaten ‘on the go’ will differ dramatically from food which can be consumed when seated.  Also components of foods may convey quality specific to a food group; fat is an important quality to look for in meat cuts, but is redundant when choosing fruit or vegetables.
With each new food or flavour experience quality perception changes and may affect previous and future expectations and experiences. A beer from a large multinational brewer may taste great, but after consumption of fine hand-pulled ale from a small local producer your tastes and expectations evolve.  In most cases more than one exposure to novel foods and flavours are required for appreciation.  New flavours, methods of cooking or preparation and increased knowledge concerning food products, ingredients and health claims can also alter perception.
Emerging food trends such as lowered fat products are viewed as quality by some, yet despised by others who perceive quality not through fat content but prefer foods embedded within traditions and taste. Food quality perception is a subjective experience which is definable, only by the individual. What rates high on one’s quality list, will not appear on another’s.  The subjectivity and argue-ability of the quality of a food makes the topic inherently interesting. 

The above words are adapted from a Chapter I wrote titled ‘Food Quality Perception’ in Processing Effects on Safety and Quality of Foods, Editor Ortega-Rivas. Publisher Taylor and Francis
Bibliography
Grunert, KG. 1997. What's in a steak? A cross-cultural study on the quality perception of beef. Food Quality and Preference 8 (3):157-174.
———. 2002. Current issues in the understanding of consumer food choice. Trends in Food Science and Technology 13:275-285.
Grunert, KG, K Bredahl, and K Brunso. 2003. Consumer perception of meat quality and implication for product development in the meat sector - a review. Meat Science 66:259-272.
Holm, L, and H Kildevang. 1996. Consumers' views on food quality. A qualitative interview study. Appetite 27 (1):1-14.
Hyde, RJ, and SA Witherly. 1993. Dynamic contrast: a sensory contribution to palatability. Appetite 21:1-16.
Jaeger, SR. 2006. Non-sensory factors in sensory science research. Food Quality and Preference 17:132-144.
Prescott, J. 1999. Flavour as a psychological construct: implications for perceiving and measuring the sensory qualities of foods. Food Quality and Preference 10:349-356.
Stefani, G, D Romano, and A Cavicchi. 2006. Consumer expectations, liking and willingness to pay for speciality foods: Do sensory characteristics tell the whole story? Food Quality and Preference 17:53-62.


Thursday, November 22, 2012

MSG Part 2. Is MSG and allergen?


If MSG was in a court of law accused of causing harm, the lawyer would be screaming ‘SHOW ME THE EVIDENCE’.  Speculative reports of ill harm after consuming MSG laced foods are rife and where there is smoke there is often fire.  But an evidence trail is needed, and in the case of MSG as an allergen the evidence is missing without a trace. In 2010 I watched a TV program while on holiday in New Zealand where the presenter talked with some authority and conviction about the food additive MSG being a major problem in foods.  The presenter was a local chef and he was going to prepare some good tasting Asian food without the MSG. After the show I requested the evidence to support the MSG harm proposition from the show’s producers.  To their credit they eventually responded with data, but it was not relevant to MSG as a ‘cause of harm’ in the food supply. The producers should have checked with any of the following organisations who have extensively reviewed the topic: The Joint Expert Committee on Food Additives of the United Nations; Food and Agricultural Organization and; World Health Organisation, all who placed MSG in the safest category for food additives. Or perhaps International and National bodies for the safety of food additives including: International Food Information Council; U S Food and Drug Administration; the National Academy Sciences; the European Community’s Scientific Committee for Food; and the American Medical Association who all report MSG safe for human consumption as a flavor enhancer. In Australia, FSANZ quoted from overwhelming evidence from considerable scientific studies to explicitly deny any link between MSG and "serious adverse reactions" or "long-lasting effects", declaring MSG "safe for the general population". The problem as I see it was the producers and presenter were na├»ve regarding the topic of MSG, but would have heard anecdotal evidence from unreliable sources that MSG was bad. They then produce a harmless cooking program further propagating the myth that MSG is harmful to the general public.   
The question remains why is MSG such a public-touchstone for allergens? The history is intriguing.  In 1968, Robert Ho Man Kwok, MD described a collection of symptoms he experienced after eating Chinese food. He coined the phrase “Chinese Restaurant Syndrome” (CRS) to describe these symptoms such as hypersensitive reaction; headache; tightness in the chest; asthma; flushing; body tingling in addition to numbness at the back of the neck and a feeling of pressure in the face and upper chest muscles.  He named many potential causes from the foods eaten and among them MSG was mentioned. It was MSG amongst all other contenders that was followed up by some other speculative reports in scientific literature.  Once it made the general media the foundation was set, MSG caused CRS. (It is important to note that I am not stating people do not suffer hypersensitive response to certain foods or CRS, but believing MSG is the cause before studies were conducted was premature.)
In 1970, Morselli and Garattini examined 17 males and seven females in a well-controlled study. The researchers administered 3 g doses of MSG in 150 ml of beef broth and evaluated the subjects every 20 minutes for a three-hour period. The researchers concluded that there was no evidence that CRS was associated with the ingestion of MSG.  Four additional double blind design (neither researchers nor subjects knew if the food contained MSG) studies with subjects who believed they adversely reacted to MSG have been conducted. In all cases the data were inconsistent with subjects responding to all stimuli including those without MSG, or none, including the foods with MSG.  The results were also inconsistent, meaning they could not be reproduced. The well-controlled science is conclusive, MSG is not a problem. Taking this into account can MSG be the problem? For the vast majority of people who believe they have an allergy/hypersensitivity/CRS to MSG, the evidence trail makes that clear that MSG is not the problem. It doesn’t mean there weren’t compounds in foods that caused a reaction, but it was not MSG.  I have included a relevant bibliography at the end of this blog for those who are interested in reading the studies mentioned. 
After all the evidence presented, if you are still adamant MSG is an allergen for you and others, then avoid foods with glutamate. In most countries the food label will show whether MSG has been used as an additive. The label will bear the food additive class name (e.g., flavor enhancer), followed by either the name of the food additive (e.g. MSG), or its International Numbering System (INS) number 621.    
Some Relevant Literature
Simon RA. Additive-induced urticaria: Experience with monosodium glutamate (MSG). J. Nutr. 130:1063S-1066S, 2000.
Tarasoff, L. & Kelly, M.F. Monosodium L-glutamate: A double-blind study and review. Food and Chemical Toxicology 1993; 31:1019-1035.
Kwok, R.H.M. Chinese Restaurant Syndrome. N. Engl. J. Med; 1968:17:796.
Morselli, P.L. & Garattini, S. Monosodium glutamate and the Chinese Restaurant Syndrome. Nature 1970; 227:611-612.
Kenney, R.A. The Chinese Restaurant Syndrome: An anecdote revisited. Food and Chemical Toxicology 1986; 24(4):351-354.
Wilkin, J.K. Does monosodium glutamate cause flushing (or merely “glutamania”)? J. Amer. Acad. Dermatol 1986;15:225-230.
Geha RS, Beiser A, Ren C, Patterson R, Greenberger PA, Grammer RC, Ditto AM, Harris KE, Shaughnessy MA, Yarnold PR et al. Glutamate Safety in the Food Supply: review of alleged reaction to monosodium glutamate and outcome of a multicenter double-blind placebo-controlled study. J. Nutr 2000;130: 1058S–1062S.
European Food Information Council. The facts on Monosodium glutamate. 2002. Center for Science in the Public Interest. Food additives.
(23) Carvan M. MSG: the controversy. LEDA at Harvard Law School, 1997.
(24) Rhodes J, Alison C, Titherley JA et al. A survey of the monosodium glutamate content of foods and an estimation of the dietary intake of monosodium glutamate. Food Additives and Contaminants 1991: 8:265-274.
(25) National Academy of Sciences, National Research Council. The 1977 Survey of the
Industry on the Use of Food Additives: Estimates of Daily Intake. Vol. 3, Washington,
D.C.: National Academy Press, 1979

Friday, November 9, 2012

MSG (Monosodium glutamate) Part 1

            Monosodium glutamate, also known as sodium glutamate or MSG, is the sodium salt of glutamic-acid or glutamate, the most abundant naturally occurring non-essential amino-acids and can be found in many protein-rich food products such as meat, poultry, fish, eggs, dairy products and other plant sources. In general, protein-rich foods contain large amounts of glutamate usually bound in the muscle.  Most vegetables contain relatively meagre quantities of glutamate, certain vegetables such as peas, tomatoes, and potatoes have significant amounts of free glutamate.
Glutamic-acid was discovered and isolated from wheat gluten and identified in the year 1866, by the German chemist Karl Heinrich Leopold Ritthausen. Later in 1907 Japanese researcher Kikunae Ikeda identified the taste properties of glutamate as brown crystals left behind after the evaporation of a large amount of Kombu broth. He found that these crystals had a hard-to-describe but undeniable flavor, something he termed ‘umami’. Other descriptors used to describe the taste of glutamate are savory, broth-like or meaty.  The best way to describe the taste is similar to a chicken broth.
            When MSG is added to foods, it provides a foundation flavour for traditional salt/savoury based foods. As discussed in my previous blogs on salt taste the majority of the global populations’ consume NaCl to excess which associates with adverse health effects e.g. hypertension, disability, cardiovascular disease. As a consequence, the WHO and the health authorities of most of the countries, including the Australian Division of World Action on Salt and Health (AWASH) advocate reducing the NaCl consumption in order to combat this health burden. It is possible, even plausible that MSG may be used to replace NaCl in food. The main advantage for MSG as a replacement for NaCl in foods is that at approximately equal intensity it contains approximately one-third the amount of Na as NaCl, and appropriate use of MSG is possible to reduce sodium in foods by up to 40% without adversly influencing liking or preference of the food. So why is such an easy solution overlooked by the food industry, could it be that there is a problem with MSG?  Perhaps allergies? That is for MSG part 2.
           

Wednesday, October 24, 2012

Beer Part 1

One of the world’s oldest foods has stood the test of time.  From accidental beginnings (presumably), perhaps a mistake from leaving bread uncovered in a rain storm a few thousand years ago, to a widely consumed incredibly diverse beverage enjoyed today.
The ingredients are simple, a source of carbohydrate/sugar, water, hops, and yeast.  But each of the ingredients can be modified prior to production thereby having multiple influences on flavour. 
Carbohydrate is usually malted barley (can be wheat, sorghum, but other grains may not have appropriate enzymes to help carbohydrate and protein breakdown sugars and amino acids which yeast use during fermentation), which is roasted to various levels of colour, and adding one or more varieties of colours of malts is the basis behind a light golden beer such as American style lagers versus black beers like Guinness.  As you go from light to darker colours, flavours change, with straw-like grainy flavours, converting to caramel/malt, going to caramel/burnt flavours.  
Water is water, but throughout history the good brewing regions are associated with good sources of water. Burton-on-Trent brewing region was founded on medicinal spring water we now know as ‘hard water’ (alkaline and mineralised), that has been shown to produce higher quality darker style of ales traditionally produced there.  Water is added to the malted barley to make a sugary solution, pretty much the base for the beer, but at this stage it does not taste like beer.
The next ingredient is hops which are used for bitterness and aroma, and there are many varieties of hops.  The brewer decides what level of bitterness is required, what level of hop aroma and adds the appropriate hops at the appropriate time of wort boiling.  For bitterness, the hops must be added early in the boil to help conversion to the bitter form, while aroma hops must be added late to ensure the volatile aromas do not evaporate during the boiling. The flavour at this stage would still not resemble beer, but would have distinct bitterness, and depending on the type of aroma hops may be aromatic, fruity and floral.
The last ingredient, yeast is also vitally important.  The yeast is added to the liquid wort, a mix of sugars, amino acids, hop compounds and given the right temperature yeast will happily grow, and in doing so turn the sugars into alcohol and other compounds that add to the flavour of the beer.  The type of yeast is important, lager yeast work well at low temperatures and produce less fruity flavours, but more sulphur flavours. Ale yeasts ferment at higher temperatures and produce a more fruity/floral and alcoholic type aromas.  If you taste the product at the end of fermentation it will taste like beer, but the final product still requires maturation to settle the yeast and mellow some of the flavours.
I find it remarkable that four primary ingredients cover such a wide spectrum of flavours.  But if four ingredients isn’t enough there are others that are added to beers, for example wheat beers with added fruit (raspberry), or around Halloween Pumpkin Ales are available.  The limit to what ingredients can be added to beer is equivalent to the limits of imagination of the brewer. 
There is certainly science and a good deal of art in brewing, but the successful brewer must understand the consumer, whether that is the mass-market consumer who consistently purchases Budweiser, or the beer enthusiast who loves discovering a rare oak aged Porter.  If the final product meets expectations of the consumer, then the ingredients and brewer have accomplished their mission.  
The title to a country song sung by Tom T Hall is appropriate to finish this blog 'I like beer'. 

Thursday, October 11, 2012

Salt Taste Part 4

The food industry loves salt, it is a magic ingredient with the ability to change an unpalatable food to one that is flavoursome and appealing. As Heston Blumenthal stated, it is the most important ingredient in the kitchen. Let’s take bread as a food that uses the multiple functions of salt.  Bread produced without salt has a vastly different taste to bread produced with salt – not only taste, but the texture is different, and 99.99% of consumers prefer their bread produced with salt.  It may seem hard to believe, but bread is the single largest source of salt in our diet; yet bread is not salty like potato chips are salty.  That is because the majority of salt is bound within the matrix and unavailable to activate our taste receptors.  It is within the bread matrix that salt has some functions, salt controls growth of yeast and promotes the development of gluten structure/texture in bread, as well as adding or enhancing flavour.  As a cook, baker or food manufacturer you would be crazy not to use salt.  The reason for salts continued (increased in the case of Australia, if you trust the recent data from Australian division World Action on Salt and Health (AWASH)) use in processed foods, given the multiple health reasons not too, is the multiple positive functions salt has in the food matrix. 
            Take meat and cheese products as examples, both are high in salt and if a manufacturer was making a reformulated meat product (chicken patties or similar), reducing the salt would adversely affect texture and require other additives to replace the water-holding, protein-binding, and fat-binding functions of the salt. In cheese, additional additives would be needed to help promote good bacteria and inhibit bad bacteria during fermentation and aging.   But what compounds can replace the function of salt, and what's the cost; consumers may not be able to afford or willing to pay for a significant increase in the cost of salt reduced foods.  In addition, we must not forget the role salt plays in preservation, as it reduces water activity in foods and acts to control growth of pathogens and spoilage organism.  If salt levels are decreased, it will be necessary to use other preservatives to ensure safe foods with a reasonable shelf life.
From a food industry perspective, in addition to processing and safety challenges involved in producing low sodium foods, there is also an economic consideration. If it becomes apparent to a food manufacturer that consumers prefer a higher concentration of salt over the current concentration, salt may be added to that food at very little cost.  For example, the approximate price of salt is 34 cents/ kg, if food manufacturers wish to increase the salt concentration of bread by 5% the approximate cost would only be 0.000756 cents/100 g. Salt is very cheap and any substitute used will increase the cost of the product. Production of foods with reduced salt will require reformulation and additional associated costs of consumer testing and pilot plant tests.  Are we as consumers willing to pay the extra costs associated with reduced salt products, or are we willing to accept inferior products? Possibly not.  Are we willing to accept myriad new additives that will be needed to replace the functions of salt? Again, possibly not. While the flavour aspects of salt are undoubtedly the main reason why salt is in foods at the level it is, there are also technical reasons to maintain salt levels in foods
It is widely accepted we have a food supply that delivers to much salt for population health.  How to fix the problem is the issue.  The most effective strategy is to reduce the level of salt in manufactured foods, as they deliver 75% of dietary salt.  The food industry correctly states salt reduction is not easy to do, and there are costs involved. And we as consumers are likely unwilling to accept increased costs that will be involved with salt reduction.
One thing for certain, the last thing we need is food manufacturers increasing the current levels of salt in foods, as AWASH reported recently.  There is no need for more salt in bread, or increased levels in cereals. If voluntary food industry targets cannot be determined or met for specific foods, the next step should be to legislate maximum levels of salt in foods.  Perhaps this is needed, if so, start with bread at a maximum level of 800mg NaCl/100g bread – this is a good compromise value, the functionality the bread matrix is maintained, taste is fine and will be a significant step forward in reducing population salt intake.
As (hopefully) explained over the past 4 blogs, salt is a problem with no easy answer.