The "Melody" of Coffee

3.6 The "Melody" of Coffee
• Salivary
FOOD
PROPERTIES
33
• Aroma compounds
• Taste compounds
• Texture
• Color IN-MOUTH  ENVIRONMENT
• Appearance
• Breathing
• Mastication
• Swallowing
• Mucous layer
PSYCHO-SOCIAL
EFFECTS
• Culture
• Memories
• Expectations
• Mood
• Alertness
. Attention


Fig. 3.1 Three factors influence flavour perception. The first includes all aspects that are related solely to the food, such as the aroma-active compounds present and interactions between the food matrix and aroma compounds. The second comprises all aspects related to the in-mouth situation. This makes the person eating the food an integral part of the system being analysed, and takes account of interactions between food and consumer. Finally, psychosocial and cognitive effects modulate aroma perception

Coffee is an interesting example of olfactory preference. The remarkable preference that some consumers develop for the volatile aroma molecules liberated from mature, partially fermented, dried, roasted and ground beans of the plant are testament to the integrative nature of the olfactory preference development process. The positive preferences that are developed are presumably a consequence, in part, of neurophysiological inputs from caffeine rather than nutritive or even microfloral inputs. Coffee aroma evolves in the mouth during drinking and finishes over several minutes after swallowing, with a typical after odour in the mouth. The nose space technique is able to capture many of these dynamic processes analytically, and gives a vivid insight into aroma release and its temporal evolution in the mouth. An abbreviated selection of I I compounds that were simultaneously measured in the air exhaled through the nose during drinking of espresso coffee is shown (Fig. 3.2) using a technique termed proton-transfer reaction mass spectrometry (PTR-MS) [26, 27]. The top-left frame of Fig. 3.2 shows the in-mouth temperature measured with a tiny thermocouple in the coffee assessor's mouth. Prior to taking coffee into the mouth, the temperature was about 35 oc. As the individual sipped the coffee (at 50 s), the temperature rose immediately to 46 oc, and then decreased owing to the thermal conduction in
 in the oral cavity. After keeping the coffee in the mouth for 10 s, the temperature dropped below 40 oc. In this specific aroma evaluation, the individual assessor was instructed to keep the coffee within the mouth for a relatively long time prior

to swallowing in order to extend the measurements during the basic processes that occur in mouth. The concentration-time plots are those of compounds appearing at the indicated masses (m/z) in the nose space air: m/z 37 corresponds to the protonated water cluster, H20•H30+, present in the breath air, whether or not the person had coffee in the mouth (natural humidity in breath). This water signal acts as a marker for the regularity and stability of breathing rhythm, another important variable in the overall in-mouth experience. Though some- what arbitrary, the overall aroma development can be considered sequentially in stages. First, at the first contact of the liquid coffee with the in-mouth environment, there is an initial rise in the concentration of aromatic compounds, the first-sip aroma. Second, the concentration of the various compounds avail- able to the olfactory epithelia peaks and then decreases rapidly. Breaking these individual compounds into discrete temporal curves of concentration versus time reveals that the rate of decrease is not the same for all compounds; hence, the overall profile of the coffee aroma exposed to the olfactory epithelia, again, changes with time. The rapid decrease of the concentrations of volatile com- pounds from coffee in the breath air is believed to be a combination of various phenomena: (l) temperature dependence of the air—water partition coefficient,
(2) dilution of coffee with saliva, (3) interaction with saliva constituents and (4) adsorption and diffusion into the mucous layer. Third, when coffee is swallowed, coffee volatiles are released during the passage through the throat. The subsequent exhalation, the swallow-breath, entrains these volatiles through the nose and out through the nostrils. Accordingly, the corresponding aroma profile is called the swallow-breath aroma. For a series of compounds, high concentrations of volatiles are measured in the breath air just after swallowing. Fourth, when coffee is swallowed, the breath air continues to contain some of the coffee volatiles for several more minutes. This effect is known as the finishing or after- odour aroma. The persistence of various coffee aroma compounds in the breath air is reminiscent of coffee aroma, although it has a composition quite different from the aroma in the first sip, or the swallow breath. The breath-by-breath observations of the retronasal aroma transport of a wide variety of subjects revealed inter- and intraindividual differences and documented the need to go beyond a static aroma description. Simply describing the odorant exposure experience requires that the various compounds be measured
odorant exposure experience requires that the various compounds bc measured as an integrated and dynamic process, but the differences among subjects imply that additionally an individualised view be brought into the very first stages of flavour research—measurement of aroma exposure. The breakthroughs in meth- odologies that bring such analytical precision to studying olfactory exposure can now be brought to address a more concrete understanding of the customerk perception of food aroma in general. The analytical approaches described must now be coupled to means to evaluate the subjective aspects of flavour preference simultaneous with odorant exposure. Ultimately, studies such as the evaluation presented will enable research to acquire a better understanding of how aromas lead to preferences for specific foods. The example of coffee aroma measurement revealed inter individual differences in the manipulation of the odorant exposure related to flavour preferences. That is, individuals who reported a greater preference for coffee manipulated the concentration of aromas to increase the net concentration and duration of exposure relative to individuals who did not regularly consume coffee. These approaches were thus capable of resolving novel aspects of the variation in individual consumers. For example, coffee is prepared differently from country to country. Individual preferences, modes of preparations and serving temperatures vary within a country and even within a family. Very accurate measures are necessary to resolve these subtle differences that are nonetheless critical to preference development. Recent studies have investigated the retronasal aroma from other foods such as ice cream or banana 1281. In all of these studies, a dynamic evolution was observed that was characteristic for the type of food and consumption temperature, and that revealed inter-individual differences. With methods in place to measure volatile aroma compounds within the ol- factory space of individuals in real time, and to couple these to subjective reports of preference, it then becomes possible to combine these with more comprehensive measures of acute metabolism and physiology within an individual during the period when a novel food is being first perceived and olfactory preferences

Hormones That Control Your Weight

Your weight is largely controlled by hormones.

Research shows that hormones influence your appetite and how much fat you store (1, 2, 3).

Here are 9 ways to "fix" the hormones that control your weight.

1. Insulin

Insulin is a hormone produced by the beta cells of your pancreas.

It's secreted in small amounts throughout the day and in larger amounts after meals.

Insulin allows your cells to take in blood sugar for energy or storage, depending on what is needed at the time.

Insulin is also the main fat storage hormone in the body. It tells fat cells to store fat, and prevents stored fat from being broken down.

When cells are insulin resistant (very common), both blood sugar and insulin levels go up significantly.

Chronically elevated insulin levels (termed hyperinsulinemia) can lead to many health problems, including obesity and metabolic syndrome (4, 5, 6).

Overeating -- especially sugar, refined carbohydrates, and fast food -- drives insulin resistance and increases insulin levels (7, 8, 9).

Here are some tips to normalize insulin levels and improve insulin sensitivity:

• Avoid or minimize sugar: High amounts of fructose and sucrose promote insulin resistance and raise insulin levels (10, 11, 12, 13, 14, 15).
• Reduce carbohydrates: A low-carb diet can cause an immediate drop in insulin levels (16, 17, 18, 19).
• Fill up on protein: Protein actually raises insulin in the short-term. However, it should lead to long-term reductions in insulin resistance by helping you lose belly fat (20, 21).
• Include plenty of healthy fats: Omega-3 fats found in fatty fish can help lower fasting insulin levels (22).
• Exercise regularly: Overweight women who walked briskly or jogged had an improvement in insulin sensitivity after 14 weeks in one study (23, 24, 25).
• Get enough magnesium: Insulin resistant people are often low in magnesium, and magnesium supplements can improve insulin sensitivity (26, 27, 28).
• Drink green tea: Green tea may lower blood sugar and insulin levels (29, 30).

BOTTOM LINE:Insulin is the main fat storage hormone in the body. Reducing sugar intake, cutting carbs and exercise are the best ways to lower insulin levels.

2. Leptin

Leptin is produced by your fat cells.

It's considered a "satiety hormone" that reduces appetite and makes you feel full.

As a signaling hormone, its role is to communicate with the hypothalamus, the portion of your brain that regulates appetite and food intake.

Leptin tells the brain that there's enough fat in storage and no more is needed, which helps prevent overeating.

People who are overweight or obese usually have very high levels of leptin in their blood. In fact, one study found that leptin levels in obese people were 4 times higher than in people of normal weight (31).

If leptin reduces appetite, then obese people with high levels of leptin should start eating less and lose weight.

Unfortunately, in obesity the leptin system doesn't work as it should. This is referred to as leptin resistance.

When leptin signaling is impaired, the message to stop eating doesn't get through to the brain, so it doesn't realize you have enough energy stored (32, 33).

In essence, your brain thinks it is starving, so you're driven to eat.

Leptin levels are also reduced when you lose weight, which is one of the main reasons it is so hard to maintain weight loss in the long-term. The brain thinks you are starving, and pushes you to eat more (34, 35, 36).

Two potential causes of leptin resistance are chronically elevated insulin levels and inflammation in the hypothalamus (5, 37, 38, 39, 40, 41).

Here are a few suggestions for improving leptin sensitivity:

• Avoid inflammatory foods: Limit foods that cause inflammation, especially sugary drinksand trans fats.
• Eat certain foods: Eat more anti-inflammatory foods, such as fatty fish (42).
• Exercise regularly: Moderate activity can improve leptin sensitivity (43, 44, 45).
• Get enough sleep: Studies have shown that insufficient sleep leads to a drop in leptin levels and increased appetite (46, 47).
• Supplements: In one study, women on a weight-loss diet who took alpha-lipoic acid and fish oil lost more weight and had a smaller decrease in leptin than those in a control group (48).

BOTTOM LINE:People with obesity tend to be resistant to the effects of leptin. Consuming anti-inflammatory foods, exercising and getting enough sleep may improve leptin sensitivity.

3. Ghrelin

Ghrelin is known as a "hunger hormone." When your stomach is empty, it releases ghrelin, which sends a message to the hypothalamus telling you to eat (49).

Normally, ghrelin levels are highest before eating and lowest about an hour after you've had a meal.

However, in overweight and obese people, fasting ghrelin levels are often lower than in people of normal weight (50, 51).

Studies have also shown that after obese people eat a meal, ghrelin only decreases slightly. Because of this, the hypothalamus doesn't receive as strong of a signal to stop eating, which can lead to overeating (52).

Here are a few tips to improve the function of ghrelin:

• Sugar: Avoid high-fructose corn syrup and sugar-sweetened drinks, which can impair ghrelin response after meals (53, 54).
• Protein: Eating protein at every meal, especially breakfast, can reduce ghrelin levels and promote satiety (55, 56, 57, 58).

BOTTOM LINE:Eating plenty of protein and avoiding foods and beverages high in sugar can help optimize ghrelin levels.

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4. Cortisol

Cortisol is a hormone produced by the adrenal glands.

It's known as a "stress hormone" because it's released when your body senses stress.

Like other hormones, it's vital to survival. However, chronically elevated levels of cortisol can lead to overeating and weight gain (59).

It appears that women who carry excess weight around the middle respond to stress with a greater increase in cortisol (60, 61).

However, a strict diet can also raise cortisol. In one study, women who consumed a low-calorie diet had higher cortisol levels and reported feeling more stressed than women who ate a normal diet (62).

These strategies can reduce cortisol levels:

• Balanced diet: Follow a balanced, real food-based diet. Don't cut calories to extremely low levels.
• Meditate: Practicing meditation can significantly reduce cortisol production (63).
• Listen to music:. Researchers report that when soothing music is played during medical procedures, cortisol doesn't rise as much (64, 65).
• Sleep more: One study found that when pilots lost 15 hours of sleep over the course of a week, their cortisol levels increased by 50-80% (66).

BOTTOM LINE:High cortisol levels can increase food intake and promote weight gain. Eating a balanced diet, managing stress and sleeping more can help normalize cortisol production.

5. Estrogen

Estrogen is the most important female sex hormone.

It is mainly produced by the ovaries, and is involved in regulating the female reproductive system.

Both very high and low levels of estrogen can lead to weight gain. This depends on age, action of other hormones, and overall state of health.

To maintain fertility during the reproductive years, estrogen starts promoting fat storage at puberty (67).

Additionally, it may stimulate fat gain in the first half of pregnancy (67).

Obese women tend to have higher estrogen levels than normal weight women, and some researchers believe this is due to environmental influences (68).

During menopause, when estrogen levels drop because less is produced in the ovaries, the site for fat storage shifts from the hips and thighs to visceral fat in the abdomen. This promotes insulin resistance and increases disease risk (69, 70).

These nutrition and lifestyle strategies can help manage estrogen:

• Fiber: Eat plenty of fiber if you want to reduce estrogen levels (71, 72, 73).
• Cruciferous vegetables: Eating cruciferous vegetables may have beneficial effects on estrogen (74, 75).
• Flax seeds: Although the phytoestrogens in them are controversial, flax seeds appear to have beneficial effects on estrogen in most women (76, 77).
• Exercise: Physical activity can help normalize estrogen levels in both premenopausal and postmenopausal women (78, 79).

BOTTOM LINE:When estrogen levels are too high or low, weight gain may occur. This depends on age and other hormonal factors.

6. Neuropeptide Y (NPY)

Neuropeptide Y (NPY) is a hormone produced by cells in the brain and nervous system.

It stimulates appetite, particularly for carbohydrates, and is highest during periods of fasting or food deprivation (80, 81, 82).

Levels of neuropeptide Y are elevated during times of stress, which can lead to overeating and abdominal fat gain (82, 83, 84).

Recommendations for lowering NPY:

• Eat enough protein: Eating too little protein has been shown to increase release of NPY, which leads to hunger, increased food intake and weight gain (85).
• Don't fast for too long: Animal studies have demonstrated that very long fasts, such as over 24 hours, can dramatically increase NPY levels (86, 87, 88).
• Soluble fiber: Eating plenty of soluble prebiotic fiber to feed the friendly bacteria in the gut may reduce NPY levels (89).

BOTTOM LINE:Neuropeptide Y (NPY) stimulates hunger, particularly during fasting and times of stress. Protein and soluble fiber can help lower NPY.

7. Glucagon-Like Peptide-1 (GLP-1)

Glucagon-like peptide-1 (GLP-1) is a hormone produced in your gut when nutrients enter the intestines.

GLP-1 plays a major role in keeping blood sugar levels stable, and also makes you feel full.

Researchers believe the decrease in appetite that occurs immediately after weight loss surgery is partly due to increased production of GLP-1 (90).

In one study, men who were given a GLP-1 solution with breakfast reported feeling more satisfied and ended up eating 12% fewer calories at lunch (91).

Suggestions to increase GLP-1:

• Eat plenty of protein: High-protein foods like fish, whey protein and yogurt have been shown to increase GLP-1 levels and improve insulin sensitivity (92, 93, 94).
• Eat anti-inflammatory foods: Chronic inflammation is linked to reduced GLP-1 production (95).
• Leafy greens: In one study, women who consumed leafy green vegetables like spinachand kale experienced higher GLP-1 levels and lost more weight than the control group (96).
• Probiotics: In an animal study, a probiotic supplement increased GLP-1 levels, which led to a reduction in food intake (97).

BOTTOM LINE:GLP-1 can decrease appetite and increase weight loss. Consuming a diet high in protein and greens can help boost your levels.

8. Cholecystokinin (CCK)

Like GLP-1, cholecystokinin (CCK) is another satiety hormone produced by cells in your gut (98).

Higher amounts of CCK have been shown to reduce food intake in both lean and obese people (99, 100, 101).

Strategies to increase CCK:

• Protein: Eat plenty of protein at every meal (102).
• Healthy fat: Eating fat triggers the release of CCK (103).
• Fiber: In one study, when men ate a meal containing beans, their CCK levels rose twice as much as when they consumed a low-fiber meal (104).

BOTTOM LINE:CCK is a hormone that reduces appetite and is produced when you eat protein, fat, and fiber.

9. Peptide YY (PYY)

Peptide YY (PYY) is another gut hormone that controls appetite.

It is released by cells in the intestines and colon.

Peptide YY is believed to play a major role in reducing food intake and decreasing your risk of obesity (105, 106).

Strategies to increase PYY:

• Lower-carb diet: You should eat a lower-carb diet based on unprocessed foods in order to keep blood sugar levels stable. Elevated blood sugar may impair PYY's effects (58, 107, 108).
• Protein: Eat plenty of protein from either animal or plant sources (58, 109).
• Fiber: Eat plenty of fiber (89, 110, 111).

BOTTOM LINE:In order to increase PPY levels and reduce appetite, try avoiding processed carbohydrates and eating plenty of protein and fiber.

10. Anything Else?

Hormones work together to increase or decrease appetite and fat storage.

If the system doesn't work properly, you may find yourself struggling with weight issues on an ongoing basis.

Fortunately, diet and lifestyle changes can have powerful effects on these hormones.

GDP and Obesity

Female to male ratio of obesity correlates inversely with gross domestic product.
obesity correlates directly proportional to  gross domestic product.

The incessant drive of the mammalian body to obtain and store energy is likely the result of a period during evolution when food was scarce (Spiegelman and Flier, 2001). Clearly, one of the more important challenges of the current decade is to enhance our understanding of the basic mechanisms of energy homeostasis in order to gain a deeper insight into the factors that influence body weight.

Whole-Body Ablation of SRC-2 Results in Dietary Fat Malabsorption

One of the key survival strategies employed by organisms appears to be responding to cellular energy depletion by activating pathways that correct the depletion . Two ways to correct cellular energy depletion are deactivation of processes that consume ATP and activation of processes that produce ATP. An ancient energy sensor, AMP-activated protein kinase (AMPK), appears to do just that, by deactivation of ATP consuming anabolic processes and activation of ATP-producing catabolic processes . Since exogenous fuel is essential for ATP synthesis, it is no surprise that AMPK also drives appetite . We show here that once the exogenous fuel is eaten, AMPK, via a previously unlinked systemic process, allows for optimal absorption of the most energy-rich fuel: dietary fat. AMPK activates the transcriptional coactivator SRC-2

Key facts

• Worldwide obesity has nearly tripled since 1975.
• In 2016, more than 1.9 billion adults, 18 years and older, were overweight. Of these over 650 million were obese.
• 39% of adults aged 18 years and over were overweight in 2016, and 13% were obese.
• Most of the world's population live in countries where overweight and obesity kills more people than underweight.
• 41 million children under the age of 5 were overweight or obese in 2016.
• Over 340 million children and adolescents aged 5-19 were overweight or obese in 2016.
• Obesity is preventable.

World Bank income group	Year	Overweight prevalence	Overweight numbers (in millions)
Global	2018	5.9 [5.0-6.8]	40.1 [34.0-46.1]
Global	2015	5.7 [5.0-6.5]	38.6 [33.5-43.6]
Global	2012	5.5 [4.9-6.2]	36.7 [32.5-40.9]
Global	2010	5.4 [4.8-6.0]	35.2 [31.5-39.0]
Global	2005	5.1 [4.6-5.6]	32.0 [28.8-35.2]
Global	2000	4.9 [4.4-5.5]	30.1 [26.6-33.6]
Global	1995	4.8 [4.2-5.5]	30.2 [26.0-34.4]
Global	1990	4.8 [4.0-5.5]	30.9 [26.0-35.8]
Low-income	2018	3.1 [2.4-4.0]	3.6 [2.8-4.7]
Low-income	2015	3.2 [2.5-4.1]	3.6 [2.8-4.5]
Low-income	2012	3.3 [2.6-4.2]	3.5 [2.8-4.4]
Low-income	2010	3.4 [2.7-4.3]	3.4 [2.7-4.4]
Low-income	2005	3.6 [2.8-4.6]	3.3 [2.6-4.2]
Low-income	2000	3.8 [2.9-4.9]	3.1 [2.4-4.0]
Low-income	1995	4.0 [3.0-5.4]	2.9 [2.1-3.9]
Low-income	1990	4.3 [3.0-5.9]	2.7 [1.9-3.8]
Lower-middle-income	2018	3.9 [2.4-6.3]	12.1 [7.4-19.7]
Lower-middle-income	2015	3.8 [2.5-5.7]	11.7 [7.8-17.5]
Lower-middle-income	2012	3.7 [2.6-5.1]	11.3 [8.1-15.6]
Lower-middle-income	2010	3.6 [2.7-4.8]	10.9 [8.2-14.6]
Lower-middle-income	2005	3.4 [2.7-4.4]	10.1 [7.9-12.9]
Lower-middle-income	2000	3.3 [2.4-4.5]	9.3 [6.8-12.8]
Lower-middle-income	1995	3.1 [2.0-4.9]	8.7 [5.5-13.6]
Lower-middle-income	1990	3.0 [1.6-5.4]	8.1 [4.4-14.7]
Upper-middle-income	2018	7.4 [6.3-8.6]	13.2 [11.3-15.4]
Upper-middle-income	2015	7.3 [6.3-8.3]	13.3 [11.5-15.2]
Upper-middle-income	2012	7.2 [6.4-8.1]	12.8 [11.3-14.4]
Upper-middle-income	2010	7.1 [6.4-7.9]	12.4 [11.2-13.8]
Upper-middle-income	2005	7.0 [6.4-7.6]	11.8 [10.9-12.8]
Upper-middle-income	2000	6.8 [6.4-7.3]	11.9 [11.1-12.7]
Upper-middle-income	1995	6.7 [6.2-7.2]	13.3 [12.4-14.3]
Upper-middle-income	1990	6.6 [6.0-7.2]	15.4 [14.0-16.9]
Low- and middle-income	2018	4.8 [3.7-5.8]	28.9 [22.6-35.3]
Low- and middle-income	2015	4.7 [3.9-5.6]	28.5 [23.4-33.6]
Low- and middle-income	2012	4.7 [4.0-5.4]	27.5 [23.5-31.6]
Low- and middle-income	2010	4.6 [4.0-5.2]	26.8 [23.3-30.3]
Low- and middle-income	2005	4.6 [4.0-5.1]	25.2 [22.4-28.0]
Low- and middle-income	2000	4.5 [3.9-5.1]	24.3 [21.1-27.5]
Low- and middle-income	1995	4.5 [3.8-5.3]	24.9 [20.7-29.0]
Low- and middle-income	1990	4.6 [3.7-5.5]	26.1 [21.0-31.3]
Middle-income	2018	5.2 [3.9-6.4]	25.3 [19.0-31.6]
Middle-income	2015	5.1 [4.0-6.1]	24.9 [19.9-30.0]
Middle-income	2012	5.0 [4.1-5.8]	24.0 [20.0-28.0]
Middle-income	2010	4.9 [4.2-5.6]	23.4 [20.0-26.8]
Middle-income	2005	4.7 [4.2-5.3]	21.9 [19.2-24.6]
Middle-income	2000	4.6 [4.0-5.3]	21.2 [18.1-24.3]
Middle-income	1995	4.6 [3.8-5.5]	22.0 [18.0-26.0]
Middle-income	1990	4.7 [3.6-5.7]	23.4 [18.3-28.5]
High-income	2018	7.2 [4.9-10.4]	5.0 [3.4-7.2]
High-income	2015	7.0 [4.9-9.9]	4.8 [3.4-6.9]
High-income	2012	6.7 [4.8-9.4]	4.8 [3.4-6.6]
High-income	2010	6.6 [4.7-9.1]	4.6 [3.3-6.4]
High-income	2005	6.2 [4.5-8.5]	4.3 [3.1-5.8]
High-income	2000	5.9 [4.3-7.9]	4.1 [3.0-5.5]
High-income	1995	5.5 [4.1-7.5]	4.0 [2.9-5.4]
High-income	1990	5.2 [3.8-7.2]	3.8 [2.8-5.2]