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Authors: Sarah Brewer

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Nutrition (31 page)

BOOK: Nutrition
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But it’s not just the quantity of excess fat you ‘own’ – where you store it is also important. People who inherit genes that deposit excess fat around the internal organs (known as visceral, central, truncal, apple-shaped or android obesity) are more likely to develop health problems than those who store fat around their hips (pear-shaped). This is because visceral fat is different from fat stored elsewhere in the body. It secretes hormones and free fatty acids that travel directly to your liver, where they activate genes that increase liver production of cholesterol, clotting factors and other inflammatory mediators. They also act as a signal that fat stores are full, so cells become resistant to the effects of insulin and less glucose can enter cells. In addition, when free fatty-acid levels are high, muscle cells use them as a fuel, so they burn less glucose, while liver cells use them to produce new glucose – all of these factors can contribute to impaired glucose tolerance.
For Asian men, the health risks are greatest when their waist circumference expands to greater than 90 cm (36”), while for Asian women risks increase significantly above a waist size of 80 cm (32”). For people of other ethnic origins, the risk is highest once waist size reaches 102 cm (40”) for men or 88 cm (35”) for women. Different figures arise because research has shown that Asian men and women tend to have a higher proportion of body fat to muscle than the rest of the UK population and also tend to store fat around their middle. These genetic differences lead to a greater risk of developing Type 2 diabetes and coronary heart disease at a lower waist size than people of other ethnic backgrounds.
To some extent, obesity is hereditary. If both your parents are obese, you have a 70 per cent chance of obesity too, compared with less than 20 per cent if both parents are lean. This isn’t just a question of inheriting bad genes, though; family eating habits and activity patterns are also predictors of weight gain.
Appetite versus hunger
Although doctors used to dismiss the idea that hormone imbalances could cause obesity, new research suggests that this is in fact the case. It’s not the traditional hormones that are involved, however, but newly identified substances produced by your intestinal and fat cells that influence the satiety centre in your brain. Unravelling how these hormones work, and their potential as treatments for obesity and diabetes, is one of the most important areas of nutritional research today, as the development of new drugs could help to treat or prevent the current epidemic in obesity.
Ghrelin
is a hormone produced by cells in the lining of an empty stomach. Ghrelin directly stimulates your appetite centre in the hypothalamus of the brain to produce feelings of hunger. Infusing ghrelin into the circulation has been shown to increase food intake by as much as 28 per cent. Once you start to eat, however, ghrelin levels soon fall. Eating a high glycaemic-load breakfast (e.g. white toast, sugary cereal, sweetened orange juice) lowers ghrelin levels by 41 per cent; eating a low glycaemic-load breakfast (e.g. wholegrain muesli, boiled egg, unsweetened grapefruit juice) reduces ghrelin levels by 33 per cent, while a low-calorie breakfast lowers ghrelin by just 24 per cent. The fall in ghrelin levels is linked with increasing levels of insulin, and it was recently recognized that ghrelin may help to control glucose metabolism.
Obestatin hormone
is so closely related to ghrelin that it’s coded for by the same stretch of DNA, and its existence was deduced using computer analysis of the ghrelin gene. Researchers believe that the gene codes for a protein splits to produce both ghrelin and obestatin. Obestatin is believed to counteract ghrelin and reduce hunger. Latest research suggests that impaired control of the ghrelin-obestatin system may trigger obesity and diabetes.
Leptin hormone
is produced by overstuffed adipose (fat) cells in an attempt to reduce food intake. The amount of leptin you produce is directly related to the size of your fat stores, so you’d expect that the more you weigh, the fuller you’d feel. Unfortunately, there’s a catch: as you get more and more overweight, leptin receptors in the appetite centre of your brain become less and less responsive to its effects. The satiety signal that stops you eating simply doesn’t get through. This effect is linked with insulin resistance, and people with Type 2 diabetes have higher leptin levels than those without, whether or not they are also overweight. In fact, leptin appears to be involved in insulin secretion, and having a high leptin level may predict who will go on to develop diabetes, as the development of leptin resistance appears to precede the development of insulin resistance. Regular exercise may reduce leptin resistance as well as improve insulin resistance through its effects on muscle and fat metabolism.
Cholecystokinin
(CCK) is a hormone produced in your small intestine (duodenum) when partially digested protein and fats are squirted through from the stomach. CCK acts on your gall bladder to stimulate release of bile. It also acts as a signal of satiety for the brain so you stop eating. CCK boosts the effects of leptin, and these two hormones may interact synergistically to control long-term food intake. If you chew your food thoroughly, and pause between mouthfuls, this will slow down your eating and give your brain more time to receive the CCK signal that you are full.
Glucagon-like peptide-1 (GLP-1)
is a hormone released towards the end of your small intestine (ileum) as yet another signal to reduce hunger and food intake. Interestingly, GLP-1 also stimulates release of insulin, and this effect is preserved in people with Type 2 diabetes. However, the release of GLP-1 after a carbohydrate-rich meal is lower in people who are obese than in those who are lean, which may be a genetic effect.
Oxyntomodulin
is another hormone produced in the lower small intestine (ileum) and also in the colon. Circulating levels of oxyntomodulin rise within 30 minutes of eating and remain elevated for several hours. It’s thought to work on the appetite centre of the brain, and oxyntomodulin infusion can reduce food intake by 20 per cent and levels of ghrelin by over 40 per cent.
Peptide-YY (PYY) and Pancreatic Polypeptide (PP)
are also satiety hormones released from the ileum and colon shortly after food intake. A virtually identical hormone, pancreatic polypeptide (PP) is released from the pancreas after eating, and suppresses appetite throughout most of the day. People who are obese have lower than normal levels of both hormones. Infusions of PYY can reduce food intake by 33 per cent over a 24-hour period, while those given an infusion of PP consumed 22 per cent fewer calories at an eat-all-you-can buffet two hours later.
Cortisol
is a stress hormone released from the adrenal glands during times of physical and emotional stress. It may be linked with a stress response in which you increase food intake (comfort eating). In one study, women were exposed to stressful activities and then left alone to recover with a bowl of snacks (but didn’t know their food intake was being investigated). Those whose cortisol level increased significantly in response to stress ate an average of 216 kcal afterwards, while those who coped better, and showed a lower cortisol reaction, snacked less (137 kcal). Those who responded to stress with high cortisol levels also showed a preference for sweet rather than salty snacks. On the control day, when they were not stressed, however, both groups ate similar amounts of snacks (177 kcal versus 187 kcal). This suggests that some people respond to stress by eating more, while others eat less, and cortisol may be involved. Eating and appetite is a complex behaviour: long-term stress may influence eating behaviour and lead to noticeable weight gain in some people. Exercise helps to overcome the effects of cortisol by resetting the flight-or-fight stress reaction to the rest-and-digest response. Exercise also boosts fat burning, reduces insulin resistance and triggers release of endorphins – brain chemicals that suppress hunger and increase feelings of euphoria.
The interaction between different hormones has a profound effect on hunger and food intake. What’s more, appetite control is closely linked with obesity, insulin resistance and diabetes. Despite the abundance of appetite-suppressing hormones in the body (obestatin, leptin, cholecystokinin, glucagon-like peptide-1, oxyntomodulin, peptide-YY, pancreatic polypeptide), the only two that markedly stimulate appetite – ghrelin and cortisol – seem to win every time.
Losing weight
Your daily energy requirement depends on your age, sex, level of activity and occupation, and is discussed in
Chapter 3
, where you will also find
Table 8
, which shows the average daily energy needs for men and women. Put simply, to lose excess weight, you will need to consume less energy than you need so that the deficit is met by raiding the fat deposited in your adipose stores.
Losing weight reduces your risk of developing Type 2 diabetes by as much as 58 per cent, as it improves insulin resistance and glucose tolerance. Losing just 10 kg (22 lb) in weight can reduce fasting blood-glucose levels by 50 per cent, as well as lowering blood pressure by an average of 10/20 mmHg, triglycerides by 30 per cent and harmful LDL cholesterol by 15 per cent, while increasing ‘good’ HDL-cholesterol by at least 8 per cent. As a result, for someone who is obese, losing 10 kg can reduce their overall risk of premature death by 20 per cent and the risk of a diabetes-related death by as much as 30 per cent. Even slight waist reductions of just 5 cm to 10 cm can considerably reduce your risk of a heart attack.
Types of diet
The vast majority of weight-loss diets fall into five main types: low-calorie diets, very low-calorie diets, low-fat diets, low-carbohydrate/high protein diets and low glycaemic-index diets.
Low-calorie
Low-calorie diets providing 1,000 to 1,500 kcal per day are effective for weight loss if they are followed long term, for at least six months, and can achieve an average weight loss of 8 per cent over a six- to twelve-month period. For someone weighing 100 kg, that represents a weight loss of 8 kg. It is easy to underestimate your calorie intake, however, and this method should ideally involve weighing foods, at least initially, to help you understand portion control (for example, the size of a piece of cheese that provides 120 kcal energy is smaller than most people realize). Studies that have looked at long-term outcomes and the ability to keep weight off suggest that they are less effective, though, as after three to four years the average weight loss is half that seen in shorter-term trials, at around 4 per cent of body weight (equivalent to just 4 kg for someone with a starting weight of 100 kg). These diets depend on constant vigilance and record-keeping, which is difficult to maintain long term.
Very low-calorie
Very low-calorie diets typically provide between 400 and 800 kcal per day, in the form of fortified, sweet or savoury drinks that replace between one and three meals per day. These provide the vitamins and minerals you need but restrict your energy intake. Under professional supervision, these diets can help you lose between 13 kg to 23 kg excess weight over the course of 12 to 18 weeks. Although these diets used to be considered extreme, they are now gaining medical acceptance for some people as part of an ongoing, structured, educational and behavioural support programme to change long-term eating and lifestyle habits. A meta-analysis of 29 studies investigating how well people managed to keep excess weight off, once they had lost it, found that very low-calorie diets were much more successful than a traditional calorie-controlled or low-fat diet, and helped people keep off considerably more weight at every year of follow-up – even up to five years.
NB These diets are considered safe and effective but only when used by appropriately selected individuals (usually with a BMI of 30 kg/M
2
or greater) under careful medical supervision. Do not follow this approach on your own. However, a modified form of VLCD is currently popular, known as the 5:2, or intermittent fasting diet, in which you eat a normal healthy diet for five days, and restrict calories to 500 (women) to 600 (men) calories for two days. This can safely be followed on your own.
Low-fat
Low-fat diets were originally based on the idea that, as fat supplies twice as many calories per gram as either protein or carbohydrate, cutting back on fat will cut back on calorie intake more effectively than cutting back on other food groups. Low-fat diets involve restricting your total fat intake to less than 30 per cent of energy intake, with reduction in saturated fat – typically to less than 7 per cent daily energy. In comparison, a typical Western diet provides over 35 per cent of energy in the form of fat, with 10 per cent or more calories coming from saturated fat. Moderate consumption of monounsaturated fats (olive and rapeseed oils) is encouraged, as are wholegrain carbohydrates, but refined and simple sugars are avoided. Although low-fat diets are the traditional weight-loss tools recommended by healthcare professionals, large studies suggest that low-fat diets are no better than low-calorie diets in helping people to achieve long-term weight loss, and that it is the energy restriction that helps weight loss rather than the fact that the diet is low in fat per se. After six months, average weight loss is around 5 kg in those following a low-fat diet, and 6.5 kg in those on a low-calorie diet. After 18 months, those following a low-fat diet have usually gained 0.1 kg from their starting weight, while those following a low-calorie diet tend to maintain a weight loss of 2.3 kg.
Low-fat diets are also promoted to help lower cholesterol levels and reduce the risk of coronary heart disease. However, the quality of fat consumed is just as important as the quantity, and a recent meta-analysis of six trials has shown that a high-fat Mediterranean diet improves heart-disease risk factors such as blood pressure, glucose control and cholesterol balance more effectively than a low-fat diet.
BOOK: Nutrition
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