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Definitions of ‘obese’

 

Obesity levels in the UK

Obesity and income in the UK

Obesity and geography in the UK

Obesity and job status in the UK

 

Possible causes of obesity

a) Genetic predisposition to be fat

b) The in-utero environment

c) Acquired from the mother, pre birth

d) Having fat friends 

e) Reaction to quitting smoking

f) Big-fridge anxiety, too much choice in large supermarkets

g) Psychology of food sizes

h) New food additives

i) Gut Bacteria, viruses

j) Watching too much TV 

k) Heating systems

l) Hormones and lack of sleep

 

The medical effects of poor diet and obesity

 

a) Salt

b) Sugar and fat

 

Diseases caused by obesity

a) Obesity and premature death

b) Cancer

c) Sleep apnoea

d) Vitamin D deficiency

e) Accelerated ageing

f) Type II diabetes

g) Hyperactivity, aggression

 

Financial costs of diet-induced obesity and ill health.

 

Calorie chart – what puts the weight on, what takes it off

 

Combating obesity – small personal steps

 

XXXX XXXX XXXX XXXX XXXX XXXX XXXX XXXX XXXX XXXX XXXX

 

Definitions of ‘obese’

 

Obesity is defined by one’s Body Mass Index (BMI).  The BMI is calculated by dividing weight in kilograms by height in metres squared.  A 1.9 metre tall person who weighs 90 kilograms would have a BMI of 90 / 1.9 squared, or 24.9.  A BMI of 20-25 is defined as normal, 25-30 is overweight, and over 30 is obese. 

 

The BMI index was developed by Adolphe Quetelet, a 19th century Belgian scientist.  (ABC of Obesity (ed Naveed Sattar and Mike Lean, 2007, Blackwell Publishing).  The main disadvantage of using this index is that muscular people such as rugby players can also have a high BMI.

 

Alternative markers of obesity include waist measurement, or waist to hip ratio.  Over 40’’, or 100 cm. waist, is risky for men; for women it is 35’’ or 88 cm.  Others look at the waist-to-hip ratio – ideally around 1.0 for men and 0.9 for women.  However it can be hard to get an accurate measurement of waist circumference, which may vary during the day anyway.  A person’s waist is generally smallest in the morning, and increases after a dinner meal in the evening.  Hip circumference is also increased by muscle mass as well as by fat.

 

Weight and height are more easily measured, so the BMI index remains popularly used.

 

Obesity is closely linked to a poor diet, with low levels of fresh fruit and vegetables and high intake of ‘junk food’, rich in calories, fat, salt, and sugar.  The diseases caused by obesity represent the principal costs of a poor-diet, both to the individual and to society.

 

Obesity levels in the UK

 

NOTES – 1) Girls / boys are persons aged 18 or less.

2) Where figures are not sex-specific, identical figures are given for both sexes and the figures starred*.

3) # Figures refer to girls / boys aged 11 to 15

4) Percentages who are ‘overweight’ do not include those who are ‘obese’.

 

year

Overweight women

Overweight men

Obese women

Obese men

Overweight girls

Overweight boys

Obese girls

Obese boys

Early 1970s

 

 

 

 

 

 

Under 2%*

Under 2%*

1980

39%

32%

6%*

6%*

 

 

 

 

1986

 

 

7%

12%

 

 

 

 

1992

40%

48%

 

 

 

 

 

 

1993

 

 

16.4%

13.2%

 

 

 

 

1994

 

 

 

 

 

 

 

 

1995

39%

49%

17.5%

15.5%

14%#

14%#

12.0%

10.9%

1996

 

 

18.2%

16.3%

13%#

15%#

12.0%

12.0%

1997

32.8%

42.5%

20.0%

17.6%

15%#

12%#

12.2%

12.3%

1998

 

 

21.7%

17.7%

15%#

14%#

14.0%

13.2%

1999

 

 

21.5%

19.0%

14%#

12%#

14.0%

16.2%

2000

 

 

21.8%

21.1%

 

 

14.1%

14.4%

2001

39.2%

46.6%

23.9%

21.6%

19%#

15%#

14.3%

15.7%

20021

51%

61%

23.0%

22.1%

15%#

14%

17.0%

16.9%

20033

56.5%

67.5%

23.9%

23.0%

 

17%

16.1%

17.0%

20042

51%*

51%*

24.0%

23.8%

27%

27%

17.9%

18.9%

2005

42%*

42%*

24.8%

23.1%

 

 

18.1%

18.0%

2006

38%*

38%*

24%*

24%*

 

 

16%

16%

2007

 

 

 

 

 

 

16.8%

16.9%

year

Overweight women

Overweight men

Obese women

Obese men

Overweight girls

Overweight boys

Obese girls

Obese boys

12002 16% of 2 – 15 year olds were obese.

22004 8.5%-10% of six year olds and 15%-17% of 15 year olds were obese.  27% of UK 7 – 11 year olds were overweight.

32003, 27.7% of under 11’s in the UK were overweight, 5% higher than in 1995 (Guardian 30/4/05, p.1). For boys, the overweight figures rose from 22.5% to 29.6%, and for girls, from 22.9% to 25.9%.

13.7% of children between 2 and 10 were obese in 2003, up from 9.9% in 1995. For boys aged 2 – 10, obesity figures rose, 1995 – 2003, from 9.6% to 14.9%. For girls, it rose from 10.3% to 12.5%.

 

Obesity projections for the UK

By 2050 it is estimated (projection made in 2009) that 50% of adults and 25% of children will be obese.

 

Obesity and income in the UK

 

The Food magazine, July/September 2007, p.16, noted that “Children’s obesity levels are closely linked to their family income”.

 

For the UK, 2007, girls’/boys’ obesity levels per income quintile are as below,

Income quintile

% girls obese

% boys obese

Lowest

8.2%

6.0%

2nd lowest

8.9%

5.2%

Middle

5.9%

4.5%

2nd Highest

5.6%

4.1%

Highest

3.9%

4.2%

 

Obesity and geography in the UK

 

In concordance with the link between obesity and income, the geography of obesity within the UK shows a clear link between poor areas and excess weight, and between affluent areas and slimness.

 

For 2005, the slimmest ten areas were (% obese in brackets), Kensington and Chelsea (11.5%), Westminster (11.8%), Camden (12.5%), Hammersmith and Fulham (12.7%), Wandsworth (13%), Richmond, Surrey (13.2%), Islington (13.8%), Barnet (14%), Lambeth (14.1%), and Elmbridge, Surrey 914.3%).

 

The fattest ten areas (2005) were Wansbeck, Northumberland (21.2%), Sunderland (21.2%), Barnsley, Yorkshire (21.4%), Bolsover, Derbyshire (21.4%), South Tyneside (21.4%), Sandwell, West Midlands (21.6%), Sedgefield, Durham (21.7%), Knowsley, Merseyside (21.7%), Corby, Northampton (22.1%), and Easington, Durham, 22.4%).

 

The Health Survey for England (2006) published regional figures for obesity in England, also indicating a link between obesity and low income; the wealthier south-east was slimmer than the north-east.

 

Region

% obese adults (2002)

% obese adults (2006)

% obese children (2002)

London

20.4

20.0

13.4

South East

20.3

24.0

18.2

South West

19.2

26.0

14.0

East Anglia

20.9

24.0

14.1

West Midlands

24.2

30.0

15.8

East Midlands

25.1

27.0

14.5

Yorkshire and Humberside

22.6

26.0

11.4

North West

21.6

NA

15.0

North East

23.9

28.0

18.3

England

 

22.0

 

Northern Ireland

 

24.0

 

Scotland

 

25.5

 

Wales

 

21.0

 

 

Obesity and job status in the UK

 

UK obesity is (inversely) related to social status. In 1998, 12% of professional men and 15% of professional women were obese. For those of managerial and technical status, the 1998 figures were 16% of men and 20% of women. For skilled non-manual, obesity affected 16% of men and 19% of women. For skilled manual workers, 21% of men and 26% of women were obese. For semi-skilled workers, 16% of men and 28% of women were obese. For unskilled manual workers, 19% of men and 31% of women were obese. Note that for men, obesity rates do not rise markedly as one descends the status scale of work once ‘skilled manual’ is reached, but for women, obesity rates rise fairly steadily right down to ‘unskilled manual. Heavier manual work by lower-status men probably contributes to this pattern.

 

In 2004 The Economist stated (20/11/04, p.32) that “Some 28% of [UK] women in the bottom social class are obese – twice the rate amongst those in the top class”. This edition of The Economist also noted, “Obese children, especially girls, are more likely to come from lower social groups, which also eat about 50% less fruit and vegetables than professionals do”.

 

However a report in The Independent on Sunday in 2007 (‘Young, middle class, and fat, 22 July 2007, pp.8-9) suggested the reverse, that “Children in families where household income is greater than £33,000 are significantly more likely to be overweight or obese than youngsters from families with the lowest incomes.  And in higher income households, the longer a mother worked each week, the greater the risk of the child being overweight”.  Employing a nanny whilst the mother worked made child obesity even more likely; the father’s employment hours made no difference.  Children in a working-mother household are likely to snack more and watch more TV (see below, possible causes of obesity).

 

Possible causes of obesity

 

a) Genetic predisposition to be fat.  There is a gene that promotes burning off fat.  However this theory does not explain the rapid rise in obesity worldwide since around 1980.

 

b) The in-utero environment.  This theory says the embryo detects in utero that the mother is ‘starved’, and grows up more efficient at storing calories as fat.  This does not explain why obesity levels continue to rise worldwide; obese mothers should now be having thinner children.  However the foetus develops its sense of smell and taste around the middle of pregnancy, and can then detect flavour molecules from food eaten by the mother.  Babies naturally prefer salty and sweet foods, and have an aversion to bitter earthy foods such as vegetables.  But babies exposed to vegetable type flavours during gestation may have a reduced aversion to such flavours when born.  So healthy, or unhealthy, eating habits can be passed from mother to child.  Babies aged 6 to 9 months are also receptive to new flavours and what they are fed at this time, sweet fatty foods or vegetables, may also shape future eating habits.

 

c) Acquired from the mother, pre birth.  Pregnant mothers who are overweight, and have elevated blood sugar may cause damage to their baby as sugar may pass across the placenta, particularly in the first few weeks of pregnancy.  There is even a ‘gestational;’ variety of diabetes, usually appearing in the second half of pregnancy, where the embryo’s pancreas has been damaged by high maternal blood sugar levels.

 

d) Having fat friends   If your friends are fat, so likely will you be overweight.  We are social animals and copy others.  So once a few people get obese they influence others to become likewise.

 

e) Reaction to quitting smoking  The increase in US obesity between 1980 and 2000 has been linked to US government health initiatives to reduce smoking.  The inflation-adjusted price of cigarettes in the US rose by 164% between 1980 and 2004.  As smokers are forced by financial pressures to quit, they may start eating more instead.  A study by professors Inas Rashad and Michael Grosman linked each 10% rise in the real price of cigarettes to a 2% rise in the number of obese people.

 

f) Big-fridge anxiety  Having a large fridge may encourage impulse-snacking, and is handy for accommodating those big 2 litre bottles of sugary chilled soft drinks. It also makes it easier to have a wide variety of cook-chill or frozen ready meals on hand, reducing further the need to do any home cooking.  The sight of mostly-empty shelves in a huge fridge may induce unease, tempting the householder to go on another shopping trip to the supermarket, whereas with a smaller fridge, the same amount of food already there would have made it look reasonably full.

 

g) Psychology of food   The size of portion we plan to consume, and even how we expect it to taste, is heavily influenced by factors other than our appetite and the ingredients actually in the food. For example describing a breakfast cereal as ‘containing soy’ will make people say it tastes worse, even if it actually contains no soy.  A ‘Black Forest double chocolate gateau’ will taste nicer than a ‘chocolate cake’ even if the two cakes are in fact identical.  

 

Perceived size matters more than actual size.  We pour ourselves a larger portion of orange juice if it the glass is short and wide than if it is tall and narrow.  We eat a ‘portion’ of yoghurt whether it comes in a small carton or a large one.- we appear to assume that whatever size a food item is packaged in,  that must be the appropriate size for a single eating of it.  So larger size packs induce us to eat more.  In the UK, the Food Standards Agency has proposed (2009) cutting the sizes of chocolate bars such as Mars Bars to a maximum of 50g, from the present 57 or 58g, and reducing the size of cans of sugary fizzy drinks.  This may work, so long as people don’t start eating a larger number of chocolate bars.

 

The softness, or mouth-feel, of foods also matters; we prefer, and eat, more soft foods.  Processed foods tend to be softer, as well as being more calorific, than natural foods – it is easier to eat processed foods with a spoon than it is to eat natural foods this way.  As households cook less and shift to processed foods, and buy more economy bulk-sized packages from supermarkets, obesity rises.

 

h)  New food additives   

i) What are these additives?  There has been an increase in the use of additives such as palm oil, hydrogenated fats, and fructose sugars (also labelled as glucose-fructose syrup, or HFCS, that is High Fructose Corn Syrup).  These substances are commonly added to many processed foods, including biscuits, cereals, fizzy drinks, high energy drinks, ice cream, and other desserts.

ii) Economic incentives.  From the manufacturer’s point of view there is an economic incentive to add these substances.  The price of natural sugar has risen recently.  These additives blend into food well and give an extra sweet taste compared to ordinary sugar, making such foods more appealing to the consumer.  Also, health fears about artificial, zero-calorie, sweeteners such as Aspartame, Saccharin, and Cyclamates, have also promoted the use of fructose.  

iii) Food quality incentives.  These additives also prolong the shelf life of food, by preventing ice crystal formation inside freezers, and preventing some foods from drying out; another perceived advantage for the consumer.  HFCS also adds texture, such as chewiness, to cereal bars, and gives ‘thickness’ to yoghurt and ice cream.

iv) Health issues.  Palm oil and fructose sugars tend to be obesogenic, encouraging the body to lay down fat reserves rather than burn off calories. They fail to stimulate the body to produce leptin or insulin; hormones that reduce appetite and make the body burn calories (see ‘medical effects of poor diet and obesity’ below).  Consumption of fructose (instead of glucose) therefore promotes weight gain, diabetes, increase of fat cells in the body, and high blood pressure.

Consumers have begun to be aware of these issues, and some food manufacturers have been forced to return to natural sugars.

 

i) Gut bacteria, viruses  The Economist’(6 January 2007, p.64, and 4 November 2009, p.101) reported on how the balance of bacteria in the (human and mouse) gut may regulate both fat acquisition and fat burning by the host’s body.  There appears to be a two-way feedback between host weight and gut bacterial population balances.  The balance of population between two major bacterial groups helps determine host weight because one group (Firmicutes) digests complex polysaccharides into sugars that are easier for the host to assimilate; another group (Bacteroidetes) fails to make so much energy from food available to its host.  Host weight changes in turn affect the bacterial population balance.  Another study found that chickens infected by a similar virus to the one that gives humans colds and sore throats caused them (the chickens) to gain weight, even though their diet did not change.  Some scientists believe there is a contagious virus whose main effect is to cause humans to gain weight.  Some have proposed a link to GM foods.  Others have proposed an evolutionary mechanism; in the past it would have been advantageous to have gut bacteria that promoted weight gain in the host, as food supplies were uncertain.  Now, in an age of plentiful calories, having such bacteria is a liability.

 

j) Watching too much TV   Watching TV could cause one to gain weight at the rate of a stone per year for ever hour watched a day.  Watching TV is a very sedentary occupation; people may be very absorbed by the TV so their fidgeting rate declines, so they burn fewer calories.  Additionally people may snack more whilst watching TV than if say reading, and they see adverts for junk food, encouraging more snacking. This effect was described by N Stoebele and J M de Castro (‘Television viewing is associated with an increase in meal frequency in humans’, Appetite, February 2004, pp.11-113. Here, ‘TV viewing was associated with increased meal frequency and as a result with increased daily intake of energy’

 

k) Heating systems   Never mind global warming, we already live in an environment ten or twenty degrees hotter than our great-grandparents did.  We have centrally heated houses (not a small fire in the corner of one room), heated cars, schools, and offices, even trains are now hermetically sealed and heated in winter.  We may also go outside less often.  Effectively we in Britain have cut by 50% or even 75% the temperature difference between our bodies (37 C) and the outside world, including the air we breathe.  Unless we’ve also cut the calories we consume accordingly, we’re on course for getting fatter.

 

l) Hormones and lack of sleep   Sleeping too little, either because of poor quality of sleep or because we don’t allocate enough hours to sleep, may have major long term deleterious effects on physical health.  Insufficient sleeping time has been linked, according to an article in the journal ‘Sleep’, in 2004, to obesity. Although we burn more calories when awake than asleep, too little sleep boosts levels of hormones that increase our appetite.  Sleep deprived people have higher levels of cortisol, and ghrelin, hormones that raise hunger, and lower levels of leptin, a hormone that signals to the brain that you are sated with food.  People who sleep too little often have fast lifestyles, may be stressed, and eat more snack foods and ready meals as opposed to healthier foods like vegetables that take longer to prepare.  This lifestyle would also be obesogenic.

 

The medical effects of poor diet and obesity

 

Perhaps the biggest cost of food deserts is the medical costs of a poor diet.

Dieticians recommend consumption of five portions of fruit and vegetables a day. This can include tinned, dried, or frozen fruit and vegetables, but much tinned food is high in sugar and salt. Processed foods often have high levels of fat, sugar, and salt, and may be lower in vitamins.  This is especially true for ‘ready meals’ which only need to be heated up in the oven or microwave. Dieticians recommend that such ready meals should be eaten with a serving of vegetables, but for many this would defeat the purpose of having food that is quick and almost labour-free to prepare.

 

There are three main dietary ‘villains’ that have adverse biological effects when consumed in excess; salt, sugar, and fat.

 

a) Salt.  Salt is often added to processed foods, and acts both as a preservative and a flavour-enhancer.  It is found in some foods not generally perceived as ‘salty’; for example some breakfast cereals, as well as tinned vegetables, where the water around the vegetables may be very salty.  Other foods where salt is added include bacon, bread, butter, some Chinese foods, crisps, curries, and lasagne.  The recommended maximum intake of salt for an adult is 6 grams.  To make foods appear lower in salt, some labels give the sodium content; salt is sodium chloride, and the chlorine part is the heavier, so 6 grams of salt is equivalent to 2.5 grams of sodium.  It is estimated that only 15 - 20% of our salt intake is ‘added salt’, sprinkled on the food; 80 - 85% is ‘hidden’ salt, added during the food’s manufacture.  Health publicity has reduced the average UK salt intake, from 9.5grams a day to 8.6 grams, but this is still considerably higher than the 6 grams recommended maximum; the intake actually necessary for a healthy adult is just 1.5 grams a day.

 

Salt contributes to high blood pressure (see also ‘Diseases caused by Obesity – b) High blood pressure’ below) and so to strokes, osteoporosis, and heart disease. A study by Cancer Research suggests that consuming 12g of salt a day doubles the chances of contracting stomach cancer, a disease that kills 6,400 Britons a year. If Britons reduced their salt intake to the daily recommended level of 6 grams, heart disease would fall by 40%, there would be 70,000 less heart attacks a year, and 35,000 less heart-attack deaths would occur each year in the UK (Daily Express, 27/1/04, p.32). The Guardian (Guardian II, 15/9/04, pp.2-3) quoted from CASH – Consensus Action on Salt and Health – that over-consumption of salt may be implicated in 120,000 heart attack deaths a year in the UK.  There is a genetic element, with some of us much more susceptible to salt-induced heart illness than others.

 

Excess salt intake has also been linked to stomach cancer, kidney failure, and osteoporosis.

 

b) Sugar and fat.  Our biological make up makes us very efficient at conserving calories. For over 99% of human history the problem faced by mankind was too few, not too many, calories available. Thus in times of plenty, humans tend to readily store calories away as fat, and in lean times the human body is very good at conserving those calories, making it hard to voluntarily lose weight but easy to put it on. Only in the last few decades of the twentieth century has a time of continual calorie surplus been present, at least in the developed world. Ironically, in the Western World, it is the cheapest foods that are often the calorie-richest, but also poor in vitamins and other nutrients.

 

The human body has various feedback mechanisms to regulate our weight and appetite.  When we consume sugar, the body produces insulin, a hormone that encourages cells to absorb glucose from the blood.  If this glucose were not absorbed, it would make the blood acidic, and create inflammation and damage the blood vessels.  This damage would be most severe in the small blood vessels (capillaries) in the extremities, the fingers and toes, also in the delicate blood vessels at the back of the eye.  This is why diabetes, untreated, leads to limb amputations and blindness, as the blood vessels in these parts of the body become inflamed, blood flow ceases, and gangrene and tissue decay sets in.

 

The glucose absorbed by the body’s cells, especially the fat cells, is turned into lipids.  Lipids circulating in the blood lead to fatty build up in the blood vessels (atherosclerosis), which can eventually block the vessel totally, leading to a stroke if this happens in the brain.  In the blood vessels supplying the heart, this blockage leads to a heart attack.  In other parts of the body, the blockage will lead to gangrene.  However lipids contained within cells are also toxic to those cells.  To deal with toxic lipids, the fat cells themselves produces another hormone, leptin.  Leptin has several functions, one of which is to suppress the appetite.  Leptin also encourages the body cells to burn lipids.  If there is an excess of lipids in the body, because too much fat / sugar has been consumed and not enough burnt off in exercise, the fat cells produce another hormone, adiponectin, that encourages fatty tissue to absorb and hence ‘lock away’, lipids.  However as the volume of fatty tissue grows, its production of adiponectin falls, although leptin production does not fall.  Adiponectin production may fall simply because the fatty tissue can absorb no more toxic lipids, but leptin is still useful to get rid of those lipids.

 

In times of feast and famine, before the arrival of high-energy processed foods, these negative feedback mechanisms worked well.  Early man would occasionally enjoy a glut of food; the excess fat and sugar would be burnt off, and what was not burnt off would be first converted into energy-storing but toxic lipids, and the toxicity of these lipids dealt with by locking them away in fat cells, where they could gradually be broken down to produce energy during lean periods.  In times of food glut, the leptin would limit food consumption, but as famine came, the lack of leptin would reduce the amount of energy burnt off and conserve the body’s resources.

 

Modern man faces a continuous period of ‘feast’, where the body is always being flooded with rich sugary fatty foods.  Insulin levels are frequently high, and one body response is for cells to become resistant to insulin.  Hence sugar is no longer absorbed from the blood, and is free to cause inflammation and local cell death.  This is called Diabetes II, to distinguish it from the related condition, Diabetes I, in which the body never produces the insulin in the first place.

 

A more controversial theory (The Economist, 13/3/2010, p.86) suggests the body may also become resistant to the high levels of leptin that are provoked by a sugar and fat rich diet.  Hence the body cells no longer burn the excess lipids resulting from this sugar and fat.  In this scenario, the insulin resistance of Diabetes II is actually a survival mechanism at the cellular level, because insulin would encourage the cells to take up toxic lipids, but the leptin signal to burn those lipids is not being received.  However what is good for the individual cells is bad for the body as a whole, as this results in higher blood levels of lipid and glucose.

 

Diseases caused by obesity

 

a) Obesity and premature death

 

In 2007, obesity was reckoned to have killed 30,000 a year in the UK, and being obese reduces life expectancy by an average nine years.  A person obese at age 18 is twice as likely to die before 50 as a person of normal weight. 

 

In the USA, in 2000, it is estimated that 400,000 premature deaths were caused by obesity.

 

b) High blood pressure

 

Like excess salt, excess fat can cause high blood pressure.  This occurs in three ways.  Firstly, the total length of blood vessels in the body increases as the body becomes more obese; simply put, there is more ‘body’ to send blood to.  This means more pressure needs to be exerted by the heart (the pump) to ensure that blood actually circulates round the entire system.  It’s a bit like adding some more radiators onto your central heating system; the boiler pump needs to work harder to circulate the hot water.  The heart squeezes the blood harder, and blood pressure rises.  Secondly, fat (adipose) tissue produces a hormone called angiotensin, which itself causes blood vessels to constrict and therefore raises blood pressure further.  Now it’s a bit like you not only installed extra radiators but also replaced the pipes with small-bore ones. Thirdly, excess body fat promotes the deposit of fat on artery walls, reducing their diameter yet more.  Now you not only have more radiators and small-bore pipes, but the pipes you have are also half-blocked with rust.

 

Excess blood pressure (hypertension) causes the heart to work harder, increasing the risk of a heart attack.  Not only that, the risk of blood vessels bursting is raised.  If that happens in the brain, it’s called a stroke, resulting in paralysis or death.  Burst blood vessels in the eye can cause macular degeneration and blindness, and in the extremities such as the toes, lead on to necrosis (gangrene) and amputations.

 

High blood pressure also has non-nutritional causes, such as stress; however stressed people may well feel too rushed to eat a healthy meal with fresh fruit and vegetables (which take more time to prepare).  Stressed people may also lack confidence, and therefore be unwilling to experiment with new foods and cooking techniques; reverting instead to easy microwave meals.  Poor nutrition and stress puts these people at double risk of high blood pressure.

 

c) Cancer

 

Obesity causes cancer in several different ways.

i) Body fat produces certain hormones such as oestrogen, excess levels of which can promote cancer

ii) Obesity is generally associated with low consumption of fruit and vegetables; these foods contain dietary fibre.  Lack of dietary fibre is associated with cancers of the colon, because without this fibre, food transits the digestive system more slowly.

iii) Low consumption of fruit and vegetables deprives the body of substances such as Vitamin C and other anti-oxidants which help fight cancer

iv) High consumption of pre-prepared food such as ready meals tends to raise salt intake, and high salt intake may promote oesophageal cancer.

v) Fat deposits may act as a storage area for carcinogenic chemicals ingested with food, e.g. pesticides.

vi) Excess fat in the stomach / belly area can promote gastric reflux – a brief surge of stomach fluids back up from the stomach into the lower oesophagus.  This acidic fluid causes the sensation of ‘heartburn’, but also damages the oesophagus, which unlike the stomach lacks a protective buffer against stomach acid.  That can cause cancer of the oesophagus.

 

In the UK, obesity is estimated (2009) to cause an extra 13,000 cases of cancer a year.

 

d) Sleep apnoea

 

Obesity may cause a condition called sleep apnoea, literally ‘sleep-no-breath’, where the sufferer momentarily stops breathing during sleep. Excess fat is deposited in the neck area and on the chest where it may obstruct airways and make breathing harder, especially when lying down in bed. The lack of oxygen causes a brief awakening, whereupon the sufferer then resumes breathing. The wake period may be so brief the sleeper doesn’t even realise they have woken. The problem is this scenario may recur hundreds of times a night, and no deep sleep is achieved. The sleep apnoea victim is permanently drowsy during the day, even though they spend adequate time in bed. Sleep apnoea may be very costly to society as it may be implicated in may motor vehicle crashes and factory machinery accidents.

 

e) Vitamin D deficiency

 

Obesity has also been implicated in vitamin D deficiency (Daily Mail 17/9/04, p.44), which can lead to rickets, the soft bones disease.  Excess body fat soaks up the vitamin, meaning the body has less to use for its metabolism. Compounding the problem is the tendency of fat people to exercise out of doors less, because the body can make vitamin D when exposed to sunlight.  Consumption of foods like oily fish, offal, and milk and dairy products helps the body metabolise vitamin D, but these foods are being replaced in our diet by processed foods; fish consumption in particular is falling.  Ozone depletion has led to a fear of skin cancer from sunlight, but “an average person can get 80% of the vitamin D they need from 30 minutes of having their face and forearms in the sun”, Professor Brian Wharton, Institute of Child Health, London.

 

f) Accelerated ageing

 

Obesity may also accelerate the ageing process (The Economist, 4/12/04, p.91). Obesity may cause premature shortening of the telomeres; these are molecular caps that form the ends of the chromosomes, the genetic material of living cells. Telomeres are a bit like the caps on the ends of shoelaces that stop the laces unravelling.  Telomeres naturally shorten with age (scientists aren’t totally sure why, especially as cells have an enzyme, telomerase, that repairs the telomeres).  As these telomeres unravel, the genetic material in the cell becomes compromised, and the cell may die, or worse, become cancerous. At a macroscopic level, this brings on signs of ageing such as less elastic skin, muscle and joints wear and tear, and a less active immune system.

 

g) Type II diabetes

 

A further complication of a poor diet, and of obesity, is Type-II diabetes. Unlike in Type-I diabetes, where the pancreas simply doesn’t make enough insulin, a hormone needed by the body to process and store sugar, in Type-II diabetes, the insulin is produced but the body loses sensitivity to it. This loss of sensitivity is linked to the body being regularly ‘flooded’ with insulin as refined, simple sugars, such as are found in sweets and many pre-prepared foods, are consumed. Blood sugar levels remain high, because it is the job of insulin to transport the sugar out of the blood into the body’s cells for use as an energy source. The diabetes patient becomes tired, as the cells lack their sugary energy source, their kidneys make a heroic effort to rid the blood of sugar via the urine, so they need to go to the toilet a lot, and also become very thirsty because of all the urination.

 

Eating natural fruits, nuts, and carbohydrate foods such as brown bread, entails the consumption of more complex sugars that are more slowly absorbed by the gut, so a ‘sugar-spike’ in the blood doesn’t happen. If, say, a sugary snack is eaten, blood levels of sugar do shoot up, causing the insulin ‘flood’. Even if the body’s insulin system can cope with this, the flood of insulin then depletes blood sugar levels to an extent where the brain perceives hunger, and another sugary snack is desired, perpetuating calorie intake, obesity and the peril of diabetes.

 

Diabetes may go on to cause other complications such as blindness, strokes, kidney failure, and amputations, because elevated sugar levels in the blood (ketoacidosis) create an inflammatory reaction.  This damages small capillaries, creating areas of dead tissue, especially in the extremities of the limbs and the delicate blood vessels of the eyes.  The total cost of diabetes, including all the complications, blindness etc. in 2001 to the NHS was £5.2 billion (Daily Telegraph, 21 February 2001, p.2), or 9% of the total NHS budget.  Type-I diabetes reduces life expectancy by an average 20 years, but Type-II diabetes will knock ten years off average life span.

 

Type-I was normally congenital, so seen in children, but Type-II developed in later adult life.  Now, with the low-fibre, high calorie diets becoming more common in children, Type-II is seen in ever-younger patients.  If the Type-II diabetes develops at a younger age, there is more time for these complications to also occur.  Diabetes is currently incurable, only controllable by insulin injections and careful diet.

 

Diabetes, like obesity is growing fast in the UK and also worldwide. 

 

In 1996, 1.6 million people in the UK had diabetes.

 

In 2004, 1.8 million people in the UK had diabetes; 1.5 million of these had Type-II diabetes, the version often associated with obesity.  A further 0.5 – 1.0 million people were estimated to have diabetes but not know it yet.

 

By the end of  2008, 2.5 million people in the UK had been diagnosed with diabetes, and it was estimated that a further 0.5 million had the disease but were unaware of it.  The breakdown for the regions of the UK was as follows (The Times, 28 October 2008, p.9)

Region

Number with diabetes (2008)

% with diabetes

% increase since 2007

All UK

2,488,814

3.8

8.9

England

2,088,335

3.9

6.4

Northern Ireland

60,822

3.3

6.8

Scotland

200,669

3.7

16.7

Wales

138,988

4.4

6.0

 

In 2008, it was predicted that, by 2025, 4.2 million people in the UK would have been diagnosed with diabetes.  Many of these will be children and young adults, with what was once considered to be a middle age to older person’s condition.

 

In China and Latin America, Type-II is rising at 5% top 9% a year. For all cases of diabetes, numbers have grown from 30 million in 1985 to 177 million in 2003, 85% of which are Type-II. Without changes in diet, the WHP expects 300 million cases by 2025, half of these in Asia.

 

g) Hyperactivity, aggression

 

Processed food, including fizzy drinks, with high levels of additives, has also been implicated in hyperactivity in children and delinquency in adults. Besides possible psychological effects, food additives may create low-level allergic reactions such as a runny, stuffed-up, nose that disturbs sleep, making sufferers tired and irritable during the day. The Daily Telegraph, 3 February 2003, p.7, reported that ‘chips, pies, and sweets were to be taken off the menu at three British prisons during a study intended to reduce violence’.

 

Financial costs of diet-induced obesity and ill health.

 

The total contribution made by obesity to UK medical costs appears to be rising quite fast.  Some estimates reported in the media are given below.

 

Year estimate made

Cost of obesity to the UK economy –

£ billions

1995

1.7

1999

2.0

2001

2.5

2003

2.6

2004

7.4 to the NHS

2008

 

10 to the UK as a whole, inc. 7.7 to the NHS

 

Academic publications have provided the following estimates,

 

The Institute of Optimum Nutrition (www.ion.ac.uk), gave figures from Fairweather-Tait S J (2003, Human Nutrition and Food Research – opportunities and challenges in the post genomic era, Philosophical Transactions, Series B, Vol. 358, pp. 1709 -1727).  This stated, ‘It is estimated that the current healthcare costs of directly diet-related diseases is in the order of £13.5 billion’.

 

The Food Magazine, Vol.65, April/June 2006, p.11, provided an estimate for total obesity costs in the UK that ranged from £11.1 billion up to £18.2 billion.  This cost-range comprised the following elements:

 

Amounts in £s billions

Direct medical costs of obesity-caused diseases (NHS and private spending)  2.3 – 7.1

Social care costs for these diseases  1.0

Lost productivity  3.4

Medical, Social, and other indirect costs  3.4 – 5.7

Childhood overweight and obesity  1.0

 

Eurofood, 17 October 2007, stated (p.21) ‘It is anticipated that obesity could cost as much as £45bn a year by 2050, to pay for growing incidents (sic) of diabetes, strokes and heart disease, as well as loss of earnings by those too heavy to work’.  Eurofood does not state whether this £45bn figure is inflation adjusted – if not, it would roughly equal the Food Magazine figure of £20bn for 2006, assuming future UK inflation of around 2% – 2.5%.

 

ABC of Obesity (ed Naveed Sattar and Mike Lean, 2007, Blackwell Publishing) estimated the costs of obesity to the UK economy as between £3.5bn and £6.4bn.

 

The Times (16 September 2009, p.24) reported that obesity in the UK was contributing towards a £599.3 million annual bill for diabetes drugs.  Over 90% of the 2.4 million known diabetes cases in the UK are Type II diabetes (there are estimated to be a further 0.5 million undiagnosed diabetes cases).  Obesity is the major contributor to the rise in Type II diabetes cases.

 

Not only are the numbers of people with obesity rising in most countries, but medical costs also tend to rise faster than inflation, as new medical technology is introduced and medical salaries rise by more than general price levels.

 

Calorie chart – what puts the weight on, what takes it off

Calorie sources

Calorie content of the following foods

1 small portion of fish and chips – 685

1 spinach & avocado sandwich - 581

1 kebab & chips – 580

1 Cornish pasty - 498

1 tube of Smarties – 456

1 jacket potato with baked beans – 386

1 bowl of mushroom risotto - 345

1 almond croissant - 330

1 Snickers bar -296

1 bowl of vanilla ice cream - 298

1 KFC chicken drumstick – 296

1 Magnum Classic (ice cream) – 260

1 slice of cheesecake - 257

1 bacon sandwich – 242

1 cream cheese & smoked salmon bagel – 229

1 bowl of strawberries & cream - 228

1 packet of crisps – 225

1 jam doughnut - 220

1 slice of cake – 219

1 cup of hot chocolate – 215

1 chocolate cupcake - 204

1 pint of lager - 200

1 bowl of trifle – 193

1 pint of beer - 182

1 glass of Pimms & lemonade – 180

1 bowl of porridge + 1tablespoon of sugar - 156

1 cranberry & apple Frusli bar – 150

1 cappuccino coffee – 150

1 large glass of red wine - 150

1 slice of garlic bread – 145

1 slice of margarita pizza - 140

1 mango & passion fruit sorbet – 138

1 bowl of minestrone soup

1 vanilla ice cream cone - 120

250 ml Red Bull – 113

1 glass of Bucks Fizz – 110

2-finger Kit Kat - 106

1 chocolate biscuit - 81

1 sausage roll – 61

1 chocolate chip cookie - 55

250 ml Coca Cola – 53

1 pack of chewing gum - 50

1 small peach – 46

16 Tic Tacs - 32

250 ml Fanta ‘Zero’ – 8

 

Calorie burners

Calories burned by ONE HOUR of the following activities

Tae Bo – 953

Boxing with a punchbag - 600

Beach volleyball - 547

Inline skating – 535

Tennis - 472

Swimming (front crawl) – 454

Tai Chi – 450

Salsa dancing - 448

Jogging – 441

Playing 5-a-side football - 437

Shopping (High Street) – 390 * see below

Vigorous hill / country walking – 379

Ballroom dancing - 345

Wii Fit – 328

Raking leaves - 322

Operating a pedalo – 318

Ballet – 312

Downhill skiing – 302

Cycling, slow pace (10 km/hour) - 297

Mowing the grass (electric mower) - 292

Walking (flat) – 290

Gardening - 272

Shopping (Supermarket) – 272 * see below

Ping pong - 240

Golf, no trolley - 232

Trampoline jumping – 225

Having sex - 225

Kite flying – 206

Surfing (water, not Internet) - 205

Decorating the house - 188

Croquet – 184

Fishing - 176

Playing the violin – 170

Housework - 168

Playing the piano - 165

Washing up – 165

Preparing dinner - 154

Trivial Pursuit – 110

Ironing clothes - 90

Watching TV – 81

Kissing - 77

Sleeping – 44

 

(Figures adapted from The Times Health Club; Peta Bee et al)

 

One kilogram (about 2.2 lbs) of fat is equivalent to 7,700 calories.

Combating obesity – small personal steps

 

Major lifestyle alterations aimed at losing weight often fail, because they are too hard to keep up.  So here are a few small steps that can be taken by almost everyone to shed a few pounds over the year.

 

a) Buy some smaller dinner plates.  We judge the size of a meal not just by the amount of food but by the proportion of the plate it covers (that’s why some pub restaurants put the meal on a plate or basket stood within another plate, it makes the portion look better value).  A smaller plate will make you satisfied with a smaller meal.  However, eating lower calorie foods may make you want to eat more to compensate.  Research reported in ‘Eurofood’ (17 June 2009, p.10) indicated that people quickly learn which foods are low calorie and up the portion size to compensate. 

 

b) Postpone meals.  Eat dinner at 6.30pm and you may feel hungry again by around 9 or 10.  If you can put off eating dinner till 7.30 or 8, you may not want such a large snack later on.  At lunchtime, hungry around 12.45?  Tell yourself you’ll eat at 1.30, and maybe avoid the need for a mid-afternoon snack.

 

c) Dilute the calories.  Eat cheese with crackers, or ice cream with fruit.  Much easier than cutting out the treats altogether and the easier it is, the more you’ll stick to it.  This could be easier than eating low-fat versions, if you think they don’t taste as nice.

 

d) Eat fruit for breakfast.  Many of eat fruit with breakfast cereals, why not go the whole way and eat just fruit, or fruit with yoghurt (low sugar, preferably).  That way, you get 1 or 2 of your ‘5-a-day’ in as well.

 

e) Drink more.  A cup of tea or coffee, even with milk (semi-skimmed, hopefully) has far fewer calories than a mid-morning snack, and will kill your appetite for a bit.  Most of us don’t drink enough anyway.

 

f) Take the stairs at least partway.  If you work on the 10th floor, get out at the 8th.  If you work on the 2nd, don’t use the lift at all, stairs are probably just as quick.  And why use the lift on the way down at all?  Save the planet, lifts use a lot of electricity.

 

g) Likewise, park a little further away from the station, shops, workplace, and walk the last bit.  You may even save money; parking charges may apply close to shops but it may be free a few hundred yards away.  Park away from the school too, get the kids fit as well.  Save on congestion, frustration, and time negotiating the mini-traffic-jam twice a day near the school gates.

 

h) Go for a 45-minute evening walk.  Get to know your neighbourhood, see how it’s changing, maybe that’s more interesting than watching the soaps.  Get the kids walking as well?  A two mile walk 2 evenings out of 3 and you’re walking nearly 500 miles every year.

 

i) Walk up/down the escalator.  You’ll save a few seconds as well, 20 seconds every working day adds up to 11 hours in ten years – almost a whole extra free day.

 

j) Fidget whilst you watch TV.  Do something else whilst you’re watching, the programme isn’t really so riveting is it?  That will keep your body on the move.  If you haven’t time for exercise, do some light exercise like stepping up/down whilst TV watching – few of us complain we can’t make the time to watch our favourite programmes.

 

k) Get a partner.  Single people tend to eat less-healthy ready meals, and you can slim down much faster if you and your partner motivate each other. 

 

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