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1.0 Possible causes of obesity

1.1 Biological predispositions

a) Genetic predisposition to be fat

b) The in-utero environment

c) Acquired from the mother, pre-birth

d) Gut bacteria, viruses

1.2 Biochemistry of food

e) New food additives

1.3. Lifestyle choices

f) Having fat friends

g) Reaction to quitting smoking

h) Watching too much television

i) Eating at the wrong time

j) Heating systems

k) Hormones and lack of sleep

l) Having small children, and lack of time

1.4. Food psychology

m) Big fridge anxiety

n) Portion size, food perception

2.0. A short biology of food digestion and biological feedback mechanisms

2.1. Digestion and the basic nutrients

a) The human digestive system

b) The basic nutrients

c) Sugar

d) Fats

e) Proteins

2.2 Dietary and hormonal feedback mechanisms

a) General biological feedback principles

b) Effects of sugar in the blood

c) Effects of insulin in the body

d) Hungry?

e) Is sugar worse than fat for making you fat?

f) Fat storage and the dietary feedback system

g) A financial analogy; the role of carbohydrates, fats, and proteins

h) The brain, hedonic hunger

3.0. 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, reduced intelligence

h) Fragile bones

i) Spotty pale face



1.0 Possible causes of obesity


1.1 Biological predispositions


a) Genetic predisposition to be fat.  There is a gene that promotes burning off fat; absence of this gene, or its non-functioning, could make you fat.  However this theory alone does not explain the rapid rise in obesity worldwide since around 1980.  The genetic make up of the human race cannot change as quickly as obesity has grown.  However it is possible, likely even, that some individuals are more genetically prone to be rotund, or beanpole shaped, than others, and that some people are more prone to put on weight than others; genes may not make us fat, but in the presence of other factors they can influence just how much weight we gain or lose.


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.  Children born to Dutch mothers immediately after the famine in The Netherlands in 1944 turned out to have higher propensities to be obese; this generation also suffered raised levels of cardiovascular disease and diabetes, compared to children born a year or tow before this famine.  Recent research (reported in The Economist, 8 January 2011, p.76) suggests that having a hungry father can also produce an ‘efficient-calor0e-storing’ child.  Starvation can alter the way non-foetal cells process and store energy; the cell’s DNA itself is changed, by a process called ‘methylation’.  Experiments on mice suggest that sperm cells of starved fathers, of mice at least, are methylated’ this way, and so the foetus can detect it has been sired by a starved father, and hence adapt itself to storing calories more efficiently post-birth.


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.  But many obese persons do not (yet) have diabetes.


d) 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.  These theories are possible, but no such bacteria or virus has yet been found.


1.2. Biochemistry of food


e)  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.


1.3. Lifestyle choices


f) 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, because we copy the dietary habits of our associates.


g) 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.  Quitting smoking is also stressful, because of the intense addictive pressure faced by the smoker to re-start, and some ex-smokers cope with such stress by comfort eating, often sugary ‘feel good’ foods.


h) 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. 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’.  The advertisements people see on TV also likely has an effect – after all, if ads weren’t effective at changing consumption habits, they wouldn’t be shown.  The overwhelming majority of TV food-related adverts are for sugary junk foods, rather than healthy foods.


i) Eating at the wrong time.  Experiments on mice (Economist, 16/10/2010, p.95) suggested that exposing mice, who are nocturnal, to continuous daylight increased their tendency to eat.  Although these results are not directly transferable to (diurnal) humans, many people do extend their day, eating a large meal well after dark, (the equivalent of mice exposed to continuous light).  Not only is our waking time extended well after sunset, we expose ourselves to bright light from televisions or computer screens.  Although longer waking hours increase calorie requirements, they also boost hunger, and the eating effect outweighs the extra calories burned.  Possibly, when you consume those calories is as important for weight gain as how many calories you consume.


j) 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.  A warmer environment makes the body’s ‘brown fat’, the heat-generating, calorie-burning, fat redundant; instead we gain ‘white fat’, which is the body’s way of storing excess energy intake.  Unless we’ve also cut the calories we consume accordingly, we’re on course for getting fatter.


k) 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.


l) Having small children, and lack of time.  Research at the University of Minnesota, USA, (Dr Jerica Berge) has found that parents of young children eat more sugary junk food and have higher BMIs than child-free couples.  Lack of sleep and stress is one factor (see (k) above); lack of time to prepare healthier meals, which are usually more time-consuming to cook, is another.  Research in Birmingham, UK, (Dr Hillary Shaw, British Food Journal, forthcoming 2011/12) has also found that in the poorer areas, where low wage work predominates, the unemployed tend to be less obese and eat more fresh fruit and vegetables than those in work.  Since low-wage work can leave employees only a little better off than being unemployed, it is likely that the time-consuming effects of being in-work outweigh any positive wealth effect on healthy eating.  The unemployed are more able to access cheap street markets, at times when bargains are to be had, e.g. early on, or at close in mid-afternoon.


1.4. Food psychology


m) 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.


n) Portion size, food perception   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.


There is a comprehensive list of the multiple factors acting to promote or reduce obesity in the UK Government Report, ‘Foresight, (2007, Butland B et al), published by the Government Office for Science.


2.0.A short biology of food digestion  and biological feedback mechanisms


2.1. Digestion and the basic nutrients


a) The human digestive system.  Our digestive tract is designed to extract both the micro-and macro-nutrients from food, which we need to survive.  The main components of the human digestive system are, in order of food transit, the mouth, the oesophagus, the stomach, the small intestine, and finally the large intestine; the large intestine terminates in the anus, where excretion takes place.  The stomach completes the breakdown of food that was mechanically done in the mouth (by chewing); the breakdown in the stomach is mainly chemical, by hydrochloric acid excreted by the stomach lining.  Of course the stomach itself has a mucus lining in order to resists being digested itself by its own acid; when this lining is defective, stomach ulcers result. 


b) The basic nutrients.  The macro-nutrients of food are proteins, fats, and sugars, as well as roughage (fibre), which is not actually a nutrient but is necessary for our digestive tract to move food along properly and excrete it as faeces.  Micro-nutrients are things like vitamins and mineral elements; things like calcium to build bones, or iron to enable the blood to carry oxygen.  These are not relevant to obesity – except for the possibility that our bodies instinctively demand certain minimum levels of these micro-nutrients, and that processed food, food grown for maximum crop weight yields, has become poorer in these micro-nutrients.  In this case our bodies may be driving us to eat more, simply to get the same amounts of vitamins, minerals, as before.  This theory is as yet untested.


Most absorption of nutrients takes place in the small intestine; the large intestine is there mainly to absorb water from food, also for storage before excretion.  The nutrients absorbed by the small intestine, which include the sugars, fast, and proteins, enter the bloodstream, but do not then enter the whole body circulation immediately.  Rather, they are taken to the liver for further processing. 


It is at this stage that the complex feedback mechanism between 1) what the body has taken in, 2) what it needs for its day to day activities 3) what it will store for later use, and 4) the body’s hormonal and other feedback mechanisms, start to play out.  First, we need to explore the actual chemical nature of what the body has taken in as sugars, fats, and proteins.


c) Sugars.  Sugars are a form of carbohydrate.  Carbohydrates are compounds containing carbon, hydrogen, and oxygen, in the ration 1 carbon to 2 hydrogens and 1 oxygen; since water is composed of 2 hydrogen atoms and one oxygen atom,  the term carbo-hydrate is used.  There may be hundreds or more carbon atoms in a carbohydrate molecule, but the ratio is still 1 to 2 to 1.  The carbon atoms may be joined in the form of a chain  - - - - - - -, or a ring O, or a number of rings joined together OOOOOOO. 


Carbohydrates perform an enormous number of roles in nature.  The ‘essential oils’ that give vanilla or lemon its flavour are chain carbohydrates.  A simple sugar such as galactose, fructose or glucose is a single ring carbohydrate (O) or monosaccharide where six carbon atoms form a hexagon; as with other carbohydrates the carbon atoms are joined to each other with one, or two bonds, but as each carbon atom has four bonds available to join to other atoms with, there are always some bonds spare at each carbon atom where other atoms can be tacked on.  If the atom tacked on is another carbon atom, then it too can have further atoms joined onto it, and so on, almost ad infinitum.  That’s the wonderful thing about carbon as the basic molecule of life; because it has four bonds available, an infinite range of molecules can be formed with it and the other elements around (mostly hydrogen, nitrogen, oxygen, and a little sulphur, in the case of life on Earth).  The various sugars mentioned above differ in the precise arrangements of hydrogen and oxygen atoms joined to the basic ring of six carbon atoms.


Two such carbon rings may be joined together (OO) to form a disaccharide sugar; examples include sucrose, maltose, and lactose.  These are more complex sugars.


Carbohydrate sugars with more than two rings joined (OOOOOO...) are called polysaccharides; Starch is the commonest form of polysaccharide that is digestible by humans.  Other polysaccharides are indigestible to us, these include cellulose, the structural element of plant cell walls, and chitin, the tough material that makes up the hard outer shells of many insects.  Lignin, the basic component of wood, is also a polysaccharide.  The human digestive system cannot break these substances down into sugars; the cellulose is mainly what constitutes the roughage needed by our digestive system; however some animals, for example cows and termites, have bacteria in their digestive systems that can break down polysaccharides such as cellulose, and so can digest grass, and in the case of termites, wood.  Starch is found in potatoes, also bread, which is why if you chew on bread it starts to taste sweet, because the starch is being broken down by your saliva into sugars.


The basic lesson here is that simpler sugars, the monosaccharides, are absorbed quickly into the bloodstream by humans, but more complex sugars take longer to be digested and so are slower to raise our blood sugar level.


d) Fats.  Fats are basically fatty acids; a fatty acid is another form of carbohydrate, this time with the carbon atoms in a chain ( - - - - -  - ), and the last carbon terminates in a double bond to an oxygen atom, plus a single bond to an oxygen-hydrogen group.  That leaves this last carbon one further bond (remember. carbon has a total of four bonds to join to other atoms) with which it is joined to the string of carbon atoms behind it.


Fatty acids may be classified as saturated or unsaturated; saturated fatty acids have only single bonds between the carbon atoms in the carbon chain, this means that the maximum number of hydrogen atoms is tacked onto these carbon atoms.  Unsaturated fatty acids have double bonds between some of their carbon atoms, which means that you could add more hydrogen atoms to them by breaking one of these double bonds (leaving the carbons still joined by a single bond, which is quite good enough) and use the two broken ends of this broken bond to add a hydrogen to each end (unlike carbon, hydrogen has just one bond to join to other atoms with).  Saturated fats are chemically more stable than unsaturated.  Saturated fats have a higher melting point than unsaturated; the most unsaturated fats are liquid even at fridge temperature, whereas saturated fats are solid at room temperature.


Fatty acids are classified according to the length of the carbon chain; fewer than 6 carbon atoms is a short chain fatty acid; 6-12 is a medium chain fatty acid; 13-18 is long chain fatty acid, and over 19 is a very long chain fatty acid.


Fatty acids may also be classified as trans or cis.  Cis fatty acids have all their hydrogens tacked onto the same side of the carbon atom, but trans fatty acids have the hydrogens tacked onto both sides of the carbon chain.


Fatty acids can move fairly easily in and out of the cells in our bodies, across the cell wall that functions as the ‘border guard’ for each and every one of the trillions of cells that make up our bodies.  However within cells, a 3-carbon chain carbohydrate molecule called glycerol is used to link three fatty acids together into a molecule called a triglyceride.  Glycerol is a simple carbohydrate consisting of 3 carbon atoms in a row; its key feature is that each of these 3 carbons has an oxygen-hydrogen group (OH group) tacked on, and this OH group can be detached and replaced by a fatty acid.  This makes a much larger molecule that cannot easily get outside the cell, so triglycerides are great for immobilising fat and squirreling it away inside certain body cells,. For future use as an energy source when required  Human fat is primarily composed of such immobile triglycerides.


Fats fulfil a large number of important roles within the body.  They are a crucial part of cell walls, and on a bigger scale provide important cushioning for vital organs that otherwise might be damaged by impact with something.  Fats are crucial for the absorption of fat-soluble vitamins such as A, D, E, and K.  Fats are a major part of our brain tissue.


e) Proteins.  Proteins are more complex molecules than carbohydrates, they contain nitrogen, also a little sulphur, in addition to the carbon, hydrogen, and oxygen found in carbohydrates.  Proteins are made up of long chains of amino acids, and perform a huge variety of roles within the body, such as constituting its structures, acting as a messenger system within the body (both between and within cells), and, extremely importantly, enabling crucial chemical reactions to take place – this ‘enabling’ is called ‘catalysis’ in chemical terms.  Life on earth uses a basic set of 22 amino acids, each one of which corresponds to a set of three ‘letters’ on the DNA code that is the blueprint for every living organism on the planet.  In principle, DNA could code for up to 64 amino acids, and the range of amino acids that could exist is effectively infinite (living cells do modify some of these 22 into other types of amino acid), but on this planet at least, life uses just the 22 or so types we know of.


2.2  Dietary and hormonal feedback mechanisms


a) General biological feedback principles.  The human body does an excellent job at maintaining a constant internal environment within very narrow chemical and physical parameters, and can perform this task for a century or more, which is just as well for any slight deviation in temperature, acidity, salinity, or a thousand and one other factors would swiftly prove fatal.  Our daily diet is a supreme example of our body maintaining a constant internal environment against huge odds.  We consume hundreds of different foods, each food containing thousands of different chemicals, yet our body processes these all down into pretty much exactly the chemicals our body needs to function – try that fuelling policy with a motor car, say!  And, even for the morbidly obese, our bodies do a very good job of maintaining a constant weight, allowing for necessary growth in our earlier years.  If we suffered a daily imbalance between diet and exercise such that we put on just 20 grams a day – about the weight of twenty peanuts – by the time we reached the age of 80 we would be over 584 kilograms, well over half a ton, overweight.  Yet only two morbidly obese people in the whole world have ever exceeded this weight.


The process of using external variations upon a system in order to modify the system back towards a pre-determined state is known as negative feedback.  As we have noted, the human body does this extremely well.  The next section examines the chemical variations that our diet customarily imposes upon our internal chemical environment, and how our body uses its negative feedback mechanisms to keep our body chemistry pretty much constant.  For when it doesn’t, for when our dietary habits overwhelm these negative feedback mechanisms, or when various pathological conditions (diseases) cause the feedback mechanisms to fail, see 3.0. Diseases caused by obesity below.


b) Effects of sugar in the blood.  When sugar is absorbed by the digestive system it is in the form of simple, monosaccharide, sugars (see 2.1. c) above).  The difference between initially putting in our mouths simple sugars and more complex polysaccharide sugars (such as starch) is that the complex sugars take longer to break down into a form where as simple sugars they can enter the bloodstream.  Sugar in the bloodstream is useful as a cellular energy source but too much is detrimental to the body (as is too little).  The body regulates sugar by secreting a hormone called insulin when blood sugar levels rise too high.  If too much sugar is present in the blood, the platelets in the bloodstream become sticky, clump together, and can block the smaller capillaries that feed the body extremities such as the toes and fingers, also the delicate retina of the eye.  Excess blood sugar can also displace vitamin C in the phagocytic (bacteria-eating) white blood cells, because the chemical ‘shape’ of vitamin C is not dissimilar to glucose.  Therefore high blood glucose levels impair the immune system.  Glucose in the blood also stimulates insulin levels, which results in lower levels of growth hormones, and a depressed immune system.  Depressed phagocycte activity may promote cancer, as the phagocytes also devour cancerous cells, as well as bacteria and viruses; increased blood sugar may help cancerous tumours thrive by facilitating the tumour’s energy-producing process of anaerobic respiration; of converting glucose into lactic acid.  This inn turn acidifies the blood, causing further damage to delicate capillaries.


c) Effects of insulin in the body.  Overall then, high blood sugar is not good for the body, which is why insulin is produced, to bring blood sugar levels back to acceptable levels.  Neither is high insulin levels a good thing, so what does insulin do that is necessary in the face of higher blood sugar?  Insulin stimulates cells in the liver and muscle tissue to remove sugar from the blood and store it as glycogen.  Glycogen is a branched carbohydrate that, similarly to starch in plants, serves as an energy store for animals.  However the sites for glycogen storage in the body have only a limited capacity; when these stores are full, insulin stimulates the fat cells to take glucose from the blood and, with fatty acids, make triglycerides, which appears on us as excess fat stores.  These fat stores are saturated fats (see 2.1.d) above). 


Insulin also inhibits the action of glucagon; glucagon is a hormone that stimulates the conversion of glycogen back into glucose, so that body cells can use it for energy.  When there is no insulin in the blood, body cells do not absorb glucose from the blood, and glycogen stores are broken down into glucose; triglycerides (fat, basically) is broken down into sugars and fatty acids, providing more energy sources.  The corollary of this is that high insulin levels deter the breakdown of fatty tissue and in fact promote the storage of fat.


d) Hungry?  After some hours without eating, the liver and muscles have broken down all their glycogen into glucose; the liver produces the enzyme glycogen phosphorylase to break down its glycogen into glucose, which then passes into the bloodstream.  When the glycogen is exhausted, glucose levels in the blood begin to fall.  This can lead to hypoglycaemia, which if it goes too far can lead to brain damage and death.  Early symptoms of hypoglycaemia include restlessness (your body saying ‘get going and search for some food NOW!) and increasing feelings of unease, described by some as a sort of ‘internal trembling’.  In fact the body forestalls this, because as liver glycogen levels fall a message is sent to the hypothalamus which causes us to feel ‘hunger’.  The stomach feels empty and aches, and the urge to eat becomes inceasingly irresistible.  All this before the body has used up all its glycogen / glucose reserves, and moved onto burning fat.  This strong compulsion to eat, before fat is being burned off, is the principal reason why so many dieting efforts fail.  Especially ‘crash diets’.  Dieters have to ‘tickle the (hunger) tiger’, eating only just below the energy thay have expended, losing weight very  slowly – and coping with mild hunger feelings for months on end.


e) Is sugar worse than fat for making you fat? Complex-sugar foods are said to have a low GI (Glycaemic Index) because their sugars are only released slowly into the bloodstream.  This is biologically better because a spike in blood sugar levels, bad in itself, is followed by a spike in insulin levels, also bad.  Worse, repeated spikes in blood insulin levels may cause the body to become insensitive or resistant to insulin, which is known as Diabetes Type 2 (see 3.0 below).  Without the effects of insulin, the body cannot regulate the removal of sugar from the blood.


The interesting implication of this is that, eating fatty foods does not promote fat gain so much as eating carbohydrates, especially simple, high GI, carbohydrates, does (see Zoe Harcombe reference below).  Although fat has a higher calorific value per gram than sugar does (suggesting that eating a certain amount of fat will lead to a higher excess of calories and hence weight gain than eating the same amount of sugary foods), the biochemical pathways suggest that it is eating carbohydrates that lead to our bodies storing fat, not eating fat – if we eat fat, but not carbohydrates, our bodies sense the lack of glucose and go into fat-burning mode; if we eat sugar, our bodies go into fat-storing mode.  According to Zoe Harcombe, Atkins might have been on the right lines concerning weight control.


f) Fat storage and the dietary feedback system.  Fatty acids or 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.


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.


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.


g) A financial analogy; the role of carbohydrates, fats, and proteins.  If we regards calories to the body as analogous to income to a family, the way the body deals with its various forms of income (food and expenditures (energy needs, maintenance) is not too dissimilar to the way a family would optimise its income and outgoings. 


With a family, some of its assets are more easily convertible into ready cash, more easy to spend, than others.  Cash in the pocket is equivalent in biological terms to simple monosaccharide sugars.  Other simple disaccharide sugars are like cash in a bank current account; more or less readily convertible into cash, through a visit to the cash point.  These are the forms of money a family will spend first, just as simple sugars are what the body will draw on first for its energy requirements.  Glycogen is like an special interest savings account, higher interest, a bit less accessible, but often these sorts of accounts are limited as to how much you can squirrel away in them, like the ISA accounts in the United Kingdom.  If a family runs short of cash, and its current account balance is low, it will first draw down the balance in these special accounts.


A family short on ready cash will of course not simply look to whatever stores of less accessible capital they have ready for raiding; they will cut back on spending too.  Likewise the body can choose to cut back on its energy ‘spending’.  Energy devoted to maintaining growth, to boosting the immune system and bone density, to keeping less important tissues such as hair and skin in good condition, can all be put off for another day, just as a family short on income will put off re-roofing the house, mending the garden fence, or servicing the car.  Females very low on energy intake may find their menstrual cycle has ceased and they are temporarily infertile.  In extreme starvation, body temperature is lowered and the pulse and breathing rates also fall dramatically; just as very poor families, those affected by ‘fuel poverty’, turn down the central heating and shiver in cold homes.  A body short on calorie intake will simultaneously put out strong hunger signals, such as a rumbling tummy, shakiness, irritability, an intense preoccupation with finding food.  This is similar to a family encouraging, perhaps nagging, its most employable members to ‘get on their bikes’ and go and find work, any work, to get income coming in again.  These intense hunger signals, along with the many options that a calorie-starved body has of reducing energy requirements, are what dooms almost all dieting efforts.


Worse for those who would lose fat through dieting, the body under a sustained calorie deficit will cut back on lean tissue first; muscles will shrink, because lean tissue demands more energy maintenance than fat tissue.  Fat is too valuable an energy reserve, like the cash a family has saved for its pension, to be given up that easily.  Protein, lean tissue, is often described as financially equivalent to the very house a family lives in – surely the body will use fat before consuming, literally, itself.  Actually, protein is equivalent to, not just the house, but the furniture and paintings inside.  As mentioned above, some body tissues like skin, hair, and even bone density, are relatively expendable, in extremis..  If a family enters a prolonged period of poverty (cash / calorie deficit), they may be tempted to do two things before raiding their core savings pot, their pension for the future.  They may try and sell some antique furniture (the body shedding hair maintenance), and they may try and move to a smaller house, requiring less upkeep (the body stopping growth processes, shrinking muscles).  They may not upkeep the garden fence, even if this kept out intruders (the body cutting back on the immune system).  Only in the last resort, the very last resort, will fat be burned. 


So is fat loss just impossible?  Again, lets return to our cash-strapped family.  Let’s get them used to selling the furniture to raise cash, because no-one is working, bringing in any money wages (keeping the body short of calories from sugars).  Then, perhaps, we have shifted this family into an asset-burning way of life; they must of course in the long run balance the books by buying in second hand furniture to sell.  We have moved this family from a cash-consuming way of life to an asset-consuming way of life.  Perhaps the way to shift our bodies onto a fat burning way of life is to consume fewer sugars, but rely on fats for energy, so our bodies are moved onto a fat burning way of life, permanently.


h) The brain, hedonic hunger


A key reason why obesity is such a problem is that our ‘default mode’ is to eat, to put on weight.  Once we feel full, either due to a full stomach or due to high levels of leptin, our appetite is temporarily suppressed – BUT – we can easily desire food again if we see something nice to eat.  This is called ‘hedonic’ (pleasure-based) hunger; we don’t need to eat, our bodies don’t (immediately) need those extra calories, but we eat more nonetheless.  Again this was a useful survival mechanism in times of feast and famine; early Man might have a good harvest AND soon after, kill a large animal.  No mater that he had stuffed himself on grains, the animal kill would soon go bad, it could not be stored or refrigerated, and more importantly there was no guarantee that two ‘feast periods’ in a row would not be followed by a very prolonged ‘famine’ period.  So he ate to fullness, and then ate again.  Unfortunately no-one has told our bodies that ‘feast periods’ now come continuously, and that famine period we are insuring against by hedonic eating, piling on the pounds, will probably never come.


For an interesting analysis of the biological feedback mechanisms relating to human nutrition and obesity, read ‘The Obesity Epidemic’, Zoe Harcombe, Columbus Publishing, UK, 2010


3.0. 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)


Number with diabetes (2008)

% with diabetes

% increase since 2007

All UK








Northern Ireland













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 WHO expects 300 million cases by 2025, half of these in Asia.


g) Hyperactivity, aggression, reduced intelligence


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’.


A study at the University of Bristol also suggested that a diet of ‘junk food’, eaten by children aged under 3, could reduce their later-life IQ as compared to children who ate more fresh fruit and vegetables.  This is difficult to prove as children born to more intelligent mothers, mothers of higher social class or who are better educated, mothers who care more about their children’s health, will also likely possess higher IQs; and it is these mothers who are more likely to feed their children with healthy, fresh, foods.  Statisticians call these ‘confounding factors’, although the Bristol team claim to have controlled for these and still found an effect.  The brain grows most rapidly at age under three, so good nutrition is likely to be very significant for IQ.  If true, there is a feedback effect whereby better nourished children make more intelligent adults and parents – and more intelligent and better educated parents feed their children more nutritious food.


h) Fragile bones


Obesity in growing children can cause the skeletal system to enlarge in order to carry the extra body weight.  However unless mineral intake (e.g. calcium) is increased proportionately, the bigger bones are less dense.  This makes the child more prone to fractures, and increases the risk of osteoporosis in older age.  Unfortunately, the diet eaten by an obese child is less likely to be rich in minerals, because they are more likely to be eating the sort of junk foods that promote obesity.


i) Spotty pale face


OK, compared to cancer and diabetes this is hardly even a disease, is it?  However in our appearance-obsessed age, this might just be the trigger that gets teenagers eating more healthily.  Research at St Andrews University suggested that the way skin colour is coloured by caretenoids is judged to be more physically attractive than the same person with either pale skin or suntanned skin.  Caretenoids are the chemicals found in carrots (gives them that orange colour); they also occur in tomatoes, plums, and red peppers.  Ingest too much caretenoids and you will turn orange; however in normal quantities they give the skin a ‘golden, healthy glow’.   Caretenoids are stored in the subcutaneous fat, where they affect the skin colour.  A stroppy teenager of 16 might nor care about a risk of diabetes in thirty years time, but they might just want to look good to their mates tomorrow.  And, yes, lack of vitamin C may cause spots, as the immune system is weakened.


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