The Obesity Epidemic: What Caused It? How Can We Stop It?

by Zoe Harcombe

I believe that nature knows how to feed humans better than food manufacturers. Nature has no vested interest, no profit to be made from us and no reason to provide us with anything other than nutritious food. I therefore believe that the human race must return to eating food in the form closest to that provided by nature: meat, eggs and dairy from naturally reared animals; fish; vegetables and salads; nuts and seeds; fruits and whole grains. I call this real food.

The first law has been oversimplified: The concept of eat less/do more comes from a mistaken belief that energy in equals energy out. It follows that people are overweight because they have put too much energy in and/or expended too little energy out.

The first law of thermodynamics, even when correctly interpreted, only applies to a closed system in thermal equilibrium. The first law, therefore, cannot be applied in isolation to the human body. In an open system, not in thermal equilibrium (i.e. a human),

Why don’t we assume overweight determines energy in (heavier people need more fuel) and energy out (heavier people find it more difficult to move). Thermodynamics does not say anything about causation.

we can put a gallon of petrol into a petrol car and it will go, say, 30 miles. At this point we may be confident that energy in equals energy out. However, we can then put a gallon of diesel into the same car and it will go nowhere. Immediately we can no longer argue that energy in equals energy out.

The first and second laws of thermodynamics together tell us that, in a closed system in thermal equilibrium, energy will be conserved, but that the human being is not a closed system in thermal equilibrium, so energy will be lost and energy will be used up in making available energy.

There is some debate as to how much water is stored with glycogen, but four parts water to one part glycogen is a common and long-standing conversion.

There are two forms of fat in the human body: triglycerides and fatty acids. Human fat (adipose tissue) is stored as triglycerides. Fatty acids are burned for fuel. Triglycerides are three fatty acids bound together on a backbone of glycerol.(Glycerol is a sugar alcohol and it has many other names – glycerine, 1,2,3-trihydroxypropane etc.

Inside the fat cell, fatty acids continually ‘cycle’ across the cell membrane and back out again. Fatty acids can be used as fuel during this process (or recycled/stored if they are not used). If three fatty acids are bonded by glycerol to form a triglyceride, they can’t get back out of the fat cell until the triglyceride is broken back down into glycerol and fatty acids

If we make more glucose available to fat cells, more glycerol can be made. If more glycerol can be made, more fat is stored in the fat cells. Anything that works to transport more glucose into fat cells will lead to the conversion of more fatty acids into triglycerides and more storage of fat.

Essentially the body is in a carbohydrate/glucose/fat-storing environment or a carbohydrate-free/fatty acid/fat-burning environment.

The primary role of insulin is to return the blood glucose level to within the normal range. In performing this role, insulin converts glucose from the carbohydrate eaten into glycogen, a starch stored in the muscles and liver for energy use. If all the glycogen storage areas are full, insulin will convert the excess to fatty tissue,

type 1 diabetes was an insulin-deficient state, whereas patients with type 2 diabetes had substantial amounts of insulin in the blood and could be classified as insulin resistant.[25] Type 1 diabetes can therefore be simplistically described as the type where the pancreas does not release insulin at all. In type 2 diabetes the pancreas is effectively releasing too much insulin and yet this still fails to regulate blood glucose levels normally, as cells have become resistant to insulin.

The vast majority, 90-95%, of diabetics have type 2 diabetes.)

When type 1 diabetes occurs, sugar is lost in the urine. Indeed, diabetes means ‘sweet urine’ in Greek and diabetes is diagnosed by testing for sugar in the urine. At the 2010 Wales obesity conference Dr. Jeffrey Stephens a diabetologist, estimated that glycosuria (literally weeing out sugar in the urine) may account for 500 calories a day.

What we observe, at the onset of type 1 diabetes, is, essentially, a human body incapable of storing fat in the absence of insulin.

just as onset type 1 diabetics, before diagnosis, are unable to store fat, type 2 diabetics are masters at this. Pre-diabetic individuals are often efficient ‘fat storing machines’

doctors know that the diabetics know that insulin makes them fat.

When a non diabetic person consumes carbohydrate, insulin is released by the functioning pancreas. This has the role of: converting glucose to glycogen; facilitating the cellular uptake of glucose and converting excess glucose to fat. The lesser known hormone secreted by the pancreas is glucagon, which converts glycogen to glucose. Insulin and glucagon are working almost in equal and opposite ways to regulate blood glucose levels. When blood glucose levels rise, insulin is released to return blood glucose levels to normal. Insulin does this by turning the glucose in the blood stream into glycogen. The pancreas releases glucagon when blood glucose levels fall too low. Glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream.

The hormone glucagon also plays a key role in fat utilisation (i.e. weight loss). When there is no more glycogen available and the body requires fatty acids as an energy source, glucagon stimulates the breakdown of the triglycerides (via lipase) to release free fatty acids. (Lipase is a fat-digesting enzyme produced by the stomach, small intestine and pancreas.

An alternative driver to demand fat breakdown can be the brain. As the brain cannot use fatty acids as an energy source (unless converted to a ketone), the glycerol part of triglycerides can be converted into glucose, (via gluconeogenesis), for brain fuel.

Either the body needing fatty acids or the brain needing glucose from glycerol can encourage the breakdown of triglyceride (human fat tissue) into those component parts.

The second law also introduces the irreversibility concept. We can turn coal into heat, but we can’t turn the heat back into coal.

electricity can produce steam and steam can produce electricity, but the energy lost throughout the process is such that the electricity at the end would be a fraction of the electricity with which we began.

thermic effect of nutrients (thermogenesis) is approximately 6-8% for carbohydrate, 2-3% for fat and 25-30% for protein. [29] I.e. approximately 6-8% of the calories consumed in the form of carbohydrate are used up in digesting the carbohydrate and turning it into fuel available to be used by the body. In contrast, 25-30% of the calories consumed in the form of protein are used up in digesting the protein and turning it into fuel available to be used by the body. This also makes intuitive sense; carbohydrates are relatively easy for the body to turn into energy (indeed they start being digested, and turned into glucose, with salivary enzymes, as soon as we start chewing). Protein needs to be broken down into amino acids, which is a far more complex process.

a 2,000 calorie diet comprising 55:30:15 proportions of carbohydrate:fat:protein. This demonstrated that 2,000 calories yielded 1,848 calories available for energy. I repeated the calculation for a 10:30:60 high protein diet, as another example, and the yield drops to 1,641 calories.

The notion that a calorie is a calorie is also naive in terms of nutrition. 100 calories of tuna or pork have excellent nutritional value and complete amino acid protein representation vs. 100 calories of sugar, which have no nutritional value and no protein, let alone amino acid provision.

they put them on 2,000 calories of carbohydrate a day and they all gained weight. They then put the five people on 2,600 calories (yes – more) of fat/protein and all but one lost weight

people are not, for example, overweight because they are sedentary, but they are sedentary because they are overweight (a larger frame is quite simply more difficult to move around).

The pineal functions as a gland, secreting the hormone melatonin during the hours of darkness, which regulates the pituitary gland and is associated with the biological clock.

hours of sunlight per day and the mood aspect of serotonin play an important part in weight,

The pituitary is thus known as the master gland and this part of the brain consists of two lobes called the anterior and the posterior. The anterior releases the following hormones: human growth hormone (HGH); thyroid stimulating hormone (TSH) (to release thyroxin); adreno cortico trophic hormone (ACTH), which stimulates the adrenal cortex to produce cortisol and androgens, amongst other corticosteroids;

The main secretion from the posterior lobe is the anti-diuretic hormone (ADH).

Too much (hyper) HGH can lead to the condition crudely known as gigantism and too little (hypo) HGH can lead to the condition equally crudely known as dwarfism.

The thyroid gland secretes thyroxin, which is critical to metabolism and basal metabolic rate (BMR). We know that the thyroid gland is a clear and definite factor in weight. With no change in calories consumed, we could remove the thyroid gland in a thin person and make them fat.

(For those interested in why such stress makes you want to go to the toilet, the blood supply to the bladder and intestines is reduced – as it is needed elsewhere – and the muscular walls in these regions relax.)

The adrenal cortex produces corticosteroids such as cortisol, cortisone, corticosterone and aldosterone. The first three of these are collectively known as glucocorticoids.

the role of glucocorticoids on the utilisation of carbohydrate, fat and protein by the body.

hormone changes do drive weight changes both directly, with a metabolic impact, and indirectly, with an effect on appetite and activity levels, and that the metabolic impact is likely the greater.

estimated that 9% of adult weight gain can be attributable to prescribed medication”.

Patients should be far more vociferous and challenging before starting any medication. If the average patient knew the findings of the Glasgow review, no doubt they would think twice, even three times, before taking any medication. Doctors also need to be given more time in consultations to consider the side effects of prescription medicines. The patient leaflet for clozapine (Clozaril) says “may cause weight gain.”[46] It does not say that you may gain an average of 9.9 kilograms in one year.

Surely we have just observed the pre-requisite for an obesity epidemic? Eat less, get hungry, slow the metabolism, increase the desire to consume energy, reduce the desire to expend energy, gain weight, try to eat less and so on. We have certainly just described the western world, since we started our obsession with calorie counting.

The body’s first option, when faced with a calorie deficit, is to look for glucose in the blood stream. If we have recently eaten a carbohydrate, which has been converted into glucose, this will be used first. The body can also look for fatty acids available in the blood stream. If no energy is readily available, the body then has glucose stored, as glycogen, for this purpose. If we follow the current dietary advice to “base our meals on starchy foods”, we will eat carbohydrates in quantity and with regularity and this should optimise our glycogen storage performance within the body. This constant intake of carbohydrate should enable us to store approximately 100 grams of glycogen in the liver and 250-400 grams in the muscles. (The glycogen in the muscles can only be used by the muscles, but the glycogen in the liver can be used wherever energy is needed by the body).

If the body fails to find fuel to meet a calorie deficit, it will likely use lean tissue before fat (particularly if the calorie deficit becomes more prolonged). Lean tissue requires three times more calories than fat just to maintain itself, (“resting metabolic rates of skeletal muscle 13 kcal/kg per day and adipose tissue 4.5 kcal/kg per day”)[52] so the body needs to ‘dump’ the part of it that needs the most energy. This has a direct impact on our basal metabolic rate (need for fuel), which is counterproductive for weight loss.

Here’s a simple analogy – if we lose our job and less income is coming in to the household, we don’t automatically raid savings, we cut back on spending. If you go on a diet and less energy is coming in, the body doesn’t automatically raid fat reserves, it cuts back on the energy it expends.

significant calorie deficit will likely result in short term weight loss, particularly the first time a person attempts to ‘starve’. Weight loss becomes increasingly less successful with further attempts to restrict calorie intake, as the body has no intention of letting the same devastation happen twice. After any initial weight loss, calorie intake will need to be continually reduced to try to achieve further weight loss.

The definition of a calorie is “The amount of energy required to raise the temperature of 1 gram of water from 14.5°C to 15.5°C, at standard atmospheric pressure.”

The definition of the calorie above is, strictly speaking, the definition for the “gram calorie”. The definition for the “kilogram calorie” is the amount of energy required to raise the temperature of one kilogram of water by one degree Celsius. The Kilogram calorie is also known as: the large calorie; a food calorie and/or Calorie with a capital C. When calories are used in nutrition, and especially in food labelling, they are, strictly speaking, ‘large calories’, i.e. kilo calories, denoted by kcal as an abbreviation. However, the word kilo is invariably dropped to avoid confusion with kiloJoules and that just returns us to the word calorie.

The Calorie Formula” (also known as the calorie theory) states “One pound of fat contains 3,500 calories, so to lose 1lb a week you need a deficit of 500 calories a day.” (British Dietetic Association). There are three errors with this: 1) One pound of fat does not equal 3,500 calories; 2) The body is not a Bunsen burner; 3) There is no evidence that a repeated deficit of 3,500 calories will lead to a loss of one pound of fat. Equally there is no evidence that a repeated excess of 3,500 calories will lead to a gain of one pound of fat.

In 1901, carbohydrate, protein and fat were estimated to have 4.1, 4.1 and 9.3 calories per gram respectively[79]. (Rubner recorded the calorific value for olive oil as 9.4, so even his 9.3 was an average of four fats reviewed). This has never been a precise science. The 1911 article by Bozenraad[80] is the seminal work for the estimation of the lipid content of human fat tissue. This German article registered the fat content of adipose tissue as being anywhere from 72% to 87%, so the widely used number is the top point of the original range. Dr. Geoffrey Livesey has estimated that fat has 8.7 calories per gram.