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September 24, 2016

The physiology of adiposity

by Helene van den Berg

I, me and my fat, Part 2

A person doesn’t get fat, because they overeat, they overeat because they are getting fat. 

 Both gluttony and sloth are effects of the drive to get fatter. They are caused by a defect in the regulation of the person’s fat tissue. Like the estrogen in rats, the estrogen in women, influences an enzyme, called lipoprotein lipase (LPL). If LPL is attached to a fat cell, it will pull fat from the bloodstream into the fat cell. That person will get fatter. If the LPL is attached to a muscle cell, it pulls the fat into the muscle cell and the muscle cell burns it for fuel. 

 When estrogen levels are high, LPL activity is inhibited and less fat are accumulated in the fat cells; when estrogen levels are low, the LPL activity is upregulated and more fat is pulled from the circulation into the fat cell. By removing the ovaries, there is no estrogen and the woman gets more fat than normal, because her fat cells have more LPL doing the job. The woman now has a voracious appetite, because she is losing calories into her fat cells that are needed elsewhere to run her body. The more calories she is losing to the fat cells, the more she eats to compensate. Now a meal that would previously have satisfied her, no longer does. And because she is getting fatter and heavier, her caloric requirement increases even further. If she can’t satisfy her newfound hunger, she expends less energy….A vicious circle of fat accumulation!!.  

Estrogen inhibit the activity of LPL on fat cells.

 People get fat because of the way their fat is regulated and consequently causes gluttony ( the over- eating behavior) and physical inactivity (sloth).

 Gluttony and sloth are the EFFECT and NOT the REASON of getting fat!!.  



  • Fat tissue is meticulously regulated. Dozens of hormones and enzymes influence fat accumulation e.g. sex hormones play a role in regulating body fat, which explains why men and women fatten differently; some parts of our bodies, like the back of our hands are relatively fat free; a predisposition to fatten easily or remain lean is determined by our genes , passed from generation to generation (genetically determined regulation of fat); the amount of fat and type of fat is also carefully regulated e.g. bears/whales are naturally fat for insulation against the cold or as fuel for annual migrations or hibernations. Females will fatten in preparation for giving birth. Wild animals maintain a stable weight – and when they put on significant fat, that fat is always there for a good reason, it is never a hindrance to survival. The amount of fat in animals at any particular time of the year, is entirely regulated by biological factors. When people accumulate excess fat, something has gone wrong with the careful regulation of their fat tissue. We need to find out what the defect is and what to do about it!. 
  • Obesity can be caused by a very small, undetected defect – e.g. an environmental/genetic factor, causing a regulatory error of storing only an excess of 1% fat, can lead to obesity.
  • Whatever makes us fatter and heavier, will also make us overeat . The growth hormone in children drives spurts of a voracious appetite and periods of sloth in between. If growth is the cause and overeating the effect, it is true of our fat tissue as well. 

A study done on mice that were bred to be obese ( with obesity in their genes), have shown that they will make fat out of their food under the most unlikely circumstances, even when half starved. These rats are genetically predisposed to get fat. If they are put on a diet, they will respond by compromising its organs and muscles to satisfy its genetic drive to grow fat.  If they are to be starved to death, they will die with much of their fat tissue intact. This is also true in humans as seen in the example of the extremely poor , but overweight mothers with thin, stunted children. The mothers fat tissue will accumulate excess fat, even though the mothers are barely getting enough food to survive.

 What about habitually lean people?. They have the metabolic benefits of a body that’s programmed to be lean. Their fat tissue is regulated to not store significant calories as fat (therefore they eat less) and their muscle tissues are regulated to take up more calories to use for fuel (therefore they are more physically active). This explains why the skinny marathoners (like myself) are not lean, because they train religiously and burn off thousands of calories; rather, they are driven to expend those calories. Similarly, a  greyhound will be more active than a basset hound, not because of any conscious desire to exercise, but because its body partitions fuel to it’s lean tissue , not to it’s fat tissue. It is easier for me to believe that I remain lean, because I am so virtuous and those that get fat are not, but virtue has as little to do with our weight than with our height. When we grow taller, it’s hormones and enzymes that are promoting our growth and we consume more calories as a result.



“Lipophilia” or the “love of fat” is a term ( used by a German internist as far back a 1908), to explain why parts of our body differ in their affinity for stockpiling fat. It differs from tissue to tissue and from person to person. Genes cause obesity by directly influencing the regulation of the fat tissue/lipophilia and this regulation rules the intake of food and how energy is expended. The abnormal lipophilic tissue maintain it’s stock and may increase it, independent of the requirements of the organism – therefore the adipose tissue lives for itself!. This explains why dieting is so seldom effective and why most fat people are miserable when they fast. Constant, uncontrollable hunger is a terrible burden. Added to this is the physical discomfort, the emotional stress of being fat, the constant teasing and criticism, the accusations of gluttony and lack of will power, constant guilt feelings, which all could cause emotional disturbances. 



 We store fat to keep us warm (insulation), to protect the organs and fragile structures in our bodies and as fuel for the body. Fat is continuously flowing out of our fat cells and circulating around the body for fuel and only when it’s not used for fuel, it returns to the fat cells. This process happens regardless of whether we’ve recently eaten or exercised. Therefore the mobilization and deposition of fat go on continuously, regardless of the nutritional state of the human/animal (store calories as fat even when half starved). It is not true that carbohydrates are the preferred fuel for the body. The reason why your cells will burn carbohydrates before they will burn fat, is to keep the blood sugar levels in check after a meal. And with carbohydrate-rich diets, there is a lot of carbohydrates to be burnt, before the body gets to the fat.  During a meal, containing both fat and carbohydrates, the digested fat is sent directly to the fat cells for storage. The digested carbohydrates appear in the bloodstream as glucose. The body cells will burn this glucose for fuel. The hormone insulin keeps the blood sugar under control (Insulin is even secreted before you start eating- Pavlov response). Muscle cells store the glucose as glycogen and liver cells store some as glycogen and convert some to fat, which is stored in the fat cells. As blood sugar and insulin levels decrease, more of the stored fat during the meal, is released from the fat tissue. The more time passes after a meal (e.g. at night time), the more fat you will burn and the less glucose. Your fat cells are energy buffers!. There are two forms of fat – small fatty acids, which flows in and out of cells and larger triglycerides (composed of 3 fatty acids and a glycerol), the stored form of fat. Dozens of hormones and enzymes play a role in this process, but insulin plays the most important role. Insulin is secreted in response to carbohydrates, to keep your blood sugar under control. Insulin also regulates the use and storage of fat (fuel) and protein (building and repair). Insulin is the principal regulator of fat metabolism, through two enzymes, LPL and HSL.   

  • Lipoprotein lipase (LPL) is the enzyme that makes fat cells fatter – it pulls fat out of the bloodstream into the cells. If the LPL is on the surface of a muscle cell, it directs the fat into the muscle to be used for fuel. If it’s on a fat cell, then it makes the fat cell fatter. LPL breaks down the triglycerides in the bloodstream into their component fatty acids and then the fatty acids flow into the cell. 

With men, the LPL activity is higher in the fat tissue of the gut (“beer bellies”). As men get older, they secrete less testosterone (male sex hormone); less testosterone, means more LPL activity on the fat cells of the gut, and so more fat!.  

With women, the LPL activity is high around the hips and butt. The female sex hormone, estrogen, suppresses the activity of LPL on fat cells, therefore decreasing fat accumulation, After menopause, they secrete less estrogen and the LPL activity increases around the abdominal area, the same as in men. Pregnant women’s LPL activity increases around the butts and hips to store fat for nursing their babies, as well as balancing the weight of the child in the front of their womb. After giving birth, the LPL activity moves to the mammary glands of the breasts, to use the fat for milk production. 

LPL also explains why we don’t lose fat when we exercise. 

While we’re doing our workout, the LPL activity decreases on the fat cells and increases on the muscle cells. Fat is released from our fat tissue, for fuel in the muscle cells. Great!. We become leaner!. BUT…when we are done exercising….the LPL activity on the fat cells increases and the fat cells restock whatever fat they lost during the workout!. Bad news – we get fatter again!!. And the exercise makes us hungry and our appetite increases!. 

Insulin, is also the main regulator of LPL activity. Insulin “upregulates” LPL on the fat cells – the more insulin we secrete, the more the LPL is active on the fat cells and the more fat is diverted from the bloodstream into the fat cells,  to be stored. Insulin also suppress LPL on the muscle cells, so the muscle cells can burn blood sugar, instead of fatty acids.   

  • Hormone-sensitive lipase (HSL) – insulin also influences the enzyme, HSL. HSL works to make fat cells leaner.  It works inside the fat cells to break down triglycerides into their component fatty acids, so that the fatty acids can escape into the circulation. The more active the HSL, the more fat we liberate to burn for fuel and the less we store. Insulin suppresses HSL, preventing triglycerides from being broken down inside the fat cells. When insulin levels are elevated, fat accumulates in the fat cells. 

Insulin also increase glucose metabolism inside the fat cells, increasing the amount of glycerol molecules, which combine with fatty acids into triglycerides. More fat is stored. To have enough fat storage, insulin create new fat cells. Insulin also directs liver cells not to burn fatty acids, but to repackage them into triglycerides and send them back to the fat tissue. It even triggers the conversion of carbohydrates directly into fatty acids in the liver and in the fat tissue. 

Insulin increase the fat we store and decrease the fat we burn. 

Insulin works to make us fatter!!  

 Raised insulin levels in our bodies, has a fattening or “lipogenic effect in our body, which explains why diabetics get fatter when they take insulin therapy, independent of their food intake.


This is what happens:

You think about eating carbohydrates – you begin secreting insulin – insulin inhibits HSL and increases LPL (more fatty acids are taken into fat cells from the circulation) – you get hungry – you eat – you secrete more insulin – digested carbohydrates enter the circulation as glucose, raising blood sugar levels – secrete more insulin – diet fat is stored as triglycerides in the fat cells plus some carbohydrates are converted into fat,  in the liver – fat cells get fatter – you get fatter – the fat stays in the fat cells,  until the insulin levels drops. 

Insulin trumps the effect of other hormones, except for cortisol.  Cortisol is secreted in response to stress or anxiety. Cortisol makes us store fat both directly (by stimulating the enzyme LPL) and indirectly (by causing “insulin –resistance”, where more insulin is secreted and more fat is stored). So cortisol can make us fatter when insulin is elevated, but it can make us leaner (just like other hormones) when insulin levels are low. No wonder people get fatter, when they are stressed, anxious or depressed!. 


The BOTTOM LINE, to get leaner, is:

  • To lower our insulin levels
  • Secrete less insulin to begin with

If we can lower our insulin levels, we can burn our fat; if with elevated insulin levels in our blood, we will accumulate fat in the fat tissue. Anything that makes us secrete more insulin or keeps insulin levels elevated for longer, creates an imbalance – more fat stored, less burned – and will lead to obesity within a couple of decades…even if it as little as an excess of 20 calories /day. Insulin has another indirect effect. We depend on fatty acids for fuel after our meal, with the blood sugar returning to normal levels. If the insulin remains elevated, the fat isn’t available, nor is protein as a fuel source, which is stored away in the muscle. We can’t use the glycogen (liver/muscle) because the insulin keeps it locked up, as well. As a result the cells are starved for fuel, we feel hungry and we eat sooner or we eat more or both. Our bodies are getting bigger and our energy demand increases and we add more muscle to support the fat; our appetite for carbohydrates increases, because this is the only nutrient our cells will burn for fuel when insulin is elevated. This is a vicious cycle!!. That is why humans (animals), who become obese, are no longer able to lose weight. If we are predisposed (genetically) to get fat, we’ll be driven to crave precisely those carbohydrate-rich foods that make us fat!. 




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