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| It takes much more effort to digest and extract the energy from fat than from sweet foods but the body just loves to make and store fat, as fat is much more adept at producing energy than carbohydrates. |
After all the bad news about trans-fats, you might be relieved to know that there is one class of trans-fats which has been claimed to be actually beneficial to human health – they are known as conjugated linoleic acids (CLA) and are a family of around 30 isomers of a fatty acid known as linoleic acid.
Isomers are molecules with the identical atomic constituents of another molecule – but with the atomic bonds arranged differently.
Where CLAs differ significantly from PTFs (plant trans-fats) is that these fatty acids have both the cis and trans molecular configurations.
You can see how the double-carbon bonds of these fats are joined (or conjugated) in the diagram of a CLA, producing a molecule with both cis and trans molecular characteristics.
Whether CLAs have significant health benefits for humans is still open to debate but at least there are no identifiably negative health effects of this trans-fat.
In our diets, CLAs are present mainly in grass-fed beef, butter and mutton, although the highest concentrations are found, oddly, in kangaroo meat.
The main CLAs appear to be vaccenic acid and rumenic acid, both created by the bacterial digestion of polyunsaturated fatty acids in the biomass processed by the stomachs and intestinal tracts of ruminants.
CLAs are one of the reasons why some people stridently reject advice about the avoidance of meat and saturated fats, for there have been some interesting (but not yet fully substantiated) claims about the anti-carcinogenic, anti-obesity and anti-atherogenic properties of CLAs, mostly based on experiments with rodents and pigs.
One thing is pretty certain though – if I ever have any rats or pigs at home, and if I like them, then they will definitely get fed CLA regularly.
Diagram of a CLA showing a molecule with both cis and trans molecular characteristics.
How free fatty acids get free
As mentioned, all fats are triglycerides – meaning that all fats consist of three individual fatty acids held together (or esterified) with a glycerol backbone. The individual fatty acids are not always the same – an example triglyceride might contain palmitic acid, oleic acid and alpha-linolenic acid.
Unsaturated fats have a lower melting point compared to saturated fats – the reason is because the The double-carbon bond structures in unsaturated fats have molecular “gaps” and therefore don’t fit as snugly together as the hydrogen-saturated molecules in saturated fats.
Triglycerides can break apart under various conditions, such as bad storage, heat, digestive processes, etc – and therefore release their fatty acids as free fatty acids (FFA). Like PTFs, FFAs can have both good and bad implications for our health.
Firstly, FFAs are produced by the digestive processes and are a perfectly normal consequence of eating. Confusingly, FFAs are also produced by the body by burning stored fat in cells – but there are very highly significant differences between the two types of FFAs.
The story of how FFAs arise from the burning of body fat for energy is a fascinating subject – and they also don’t tend to cause health issues. So for the moment, we will focus only on the FFAs arising from the digestion of fats and why they might be bad for us.
How FFAs get and then lose their freedom
Despite what you might think, fats from food cannot be easily absorbed directly by the digestive system to provide energy. Instead, triglycerides need to be broken down first by pancreatic juices (specifically an enzyme called lipase activated by a protein called colipase) which function only when fats are combined with water.
Therefore, before the pancreatic juices can work, dietary fats first need to be emulsified by bile salts. Digestion of fats then occur and the triglycerides end up as a mixture of tri-, di- and monoglycerides, FFAs plus other fat soluble compounds such as vitamins and cholesterol.
This mixture forms a blend of micelles (aggregates of the digested fats and water molecules) which are then absorbed by special cells (called enterocytes) lining the small intestine – these then reconvert the micelles back into triglycerides.
Why people tend to get fat first around the belly is simply because it is where most of the body’s adipose tissues are normally located.
Yes, the digestive process converts native triglycerides from food into different glycerides and FFAs and then recombines the mix back into other triglycerides in the small gut – the difference is that the triglycerides from digestion are the types which the body actually want, for the moment.
The triglycerides resulting from digestion are then packed into chylomicrons (becoming a mix called chyle) which are then released into the capillaries of the lymph system in the intestines.
There could be huge amounts of chylomicrons floating around in the lymphatic system, enough to cause blood plasma to turn milky in colour after a fatty dinner. And then it gets even more complicated.
A gene called LPL causes the cells that line the inside of capillaries of fat (or adipose) tissues and muscles to express an enzyme called lipoprotein lipase. This enzyme digests the chylomicrons floating by and turn them into FFAs, glycerol and chylomicron remnants.
The FFAs are then absorbed by the local adipocytes (fat cells) where the FFAs are once again resynthesised into triglycerides – these final triglycerides are stored as fat droplets inside the fat cells.
The convoluted processes for digesting fats explain why the Thermic Effect of Food (TEF, or energy needed for digestion) is much higher for meats than for many carbohydrates – it simply takes much more effort to digest and extract the energy from fat than from sweet foods.
This also explains why oily fried rice is probably safer for a diabetic to consume than fluffy steamed rice – though please don’t take this as advice for diabetics to cook every-thing in oil because that is really not good either, as explained later.
Despite the high TEF of fats, it clearly does not stop many people becoming obese, or even morbidly obese – and the main reason is that the body just loves to make and store fat, as fat is much more adept at producing energy than carbohydrates.
Fat is also efficient in that it can be stored in the body in a state which does not require much water, unlike carbohydrates – and hence it is lighter.
For the same energy as from one kilo of fat, it is estimated that the body would need to store 6.75 kilos of water-bound carbohydrates – so please be (a little) thankful for fats as otherwise many people would be bigger than cows, swimming would be much more difficult and shoes will crumble after a few days unless the soles are made of metal. And we would be even more prone to high blood pressure, with CHD as an end result.
Kinds of stored human body fats
Incidentally, there are normally three kinds of stored human body fat: visceral adipose tissue (VAT, usually called abdominal fat), intramuscular fat (found in muscles) and subcutaneous fat (found under the skin). Why people tend to get fat first around the belly is simply because it is where most of the body’s adipose tissues are normally located – and the probable reason is the location is conveniently close to the small intestine where there is first access to the chylomicrons after digestion.
Remember – the body likes to make and store fat. After that, the other areas that accumulate fat easiest tend to be the skin and the bigger (but unused) muscles where lipoprotein lipase is also expressed in the capillaries. So now you know why trousers are the first adjustments on the road to obesity.
Belly pork with sweet preserved mustard and egg.
Ironically, the fat cells themselves do try to stop you overeating – and adipocytes do this by producing a hormone called leptin which is designed to turn off your urge to overeat.
But if you consume a lot of fructose (found in fruits, sweets and desserts) or have the willpower (sheer greed), then you can overcome the effect of leptin and continue overeating.
Then more fat cells will be produced, more leptin will be issued and ignored – and sooner or later, leptin resistance will develop. After that, there are very few stops left on the highway to plumpness, obesity or morbid obesity, depending on your choice of destination.
The good and bad FFAs
In moderation, there is no such thing as a good or bad natural FFA unless it is a PTF (for reasons already explained earlier). The body is capable of creating some of the fatty acids it needs to maintain health, but there are two main classes of essential fatty acids which it cannot synthesize and hence they must come from the diet – they are Omega-6 fatty acids and Omega-3 fatty acids.
The ways these polyunsaturated fatty acids work are pretty cool, but perhaps in even more convoluted fashions than the way triglycerides are digested and stored – so, to avoid boredom, the summary is as follows:
Omega-6 fatty acids: These are much more prevalent in modern diets than in Palaeolithic times due to our higher consumption of plant-based press-extracted polyunsaturated oils (eg. corn oil, soy oil, sunflower oil, etc), which would simply not be available in the past.
Omega-6 fatty acids are implicated in many important bodily functions such as brain function, anxiety, appetite control, autonomic responses, neuron functions, immune responses – and also, unfortunately, inflammation.
Too much Omega-6 has been linked to inflammation diseases such as asthma, arthritis, rheumatism, etc, caused partly by the overexpression of an enzyme called PTGS2 (Prostaglandin-endoperoxide synthase 2, also known as COX-2). A common example of an Omega-6 fatty acid is linoleic acid.
Omega-3 fatty acids: As a guess, I suppose we are consuming probably around the same amount of Omega-3 fatty acids as humans in Palaeolithic times but the ratio then was about 1:1 for Omega-6 and Omega-3 fatty acids – this is as opposed to a rough average of 15.8 times more Omega-6 than Omega-3 these days in Western countries.
This current imbalance has been associated with many modern ailments, usually linked with inflammation – and one such ailment is atherosclerosis. Omega-3 counteracts some of the effects of Omega-6 because it competes for the same enzymes and precursors as Omega-6, thus reducing the probability of the overexpression of potentially damaging enzymes such as PTGS2, for example.
Common Omega-3 fatty acids are alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) – ALA is found in nuts and plant seeds, and EPA and DHA are commonly found in certain fish oils.
And curiously, there haven’t been any major negative effects associated with the overconsumption of Omega-3 fatty acids.
The strange side-effect of FFAs
A rather odd connection has been established between the presence of FFAs in plasma, and insulin: FFAs are known to actually inhibit the action of insulin, thereby reducing the ability of skeletal muscles to remove excess glucose from the blood.
At the same time, FFAs also promote the increased production of insulin, thereby compensating for the earlier inhibitory effect. This additional insulin spike due to FFAs would probably be tolerated quite well if the diet was based on meat – but modern diets typically include a lot of refined carbohydrates and sugar (eg. burgers, pizzas, noodles, end of meal desserts, etc).
The FFA-induced spike would come on top of the carbohydrate or sugar-induced tsunami of insulin – while at the same time FFAs are also inhibiting the effect of insulin.
In the end, prolonged exposure to this unsatisfactory situation can lead to chronic insulin tolerance, Type 2 Diabetes and arterial damage due to
the persistent excess amounts of blood glucose (which can be toxic).
The situation is perhaps a little like a lousy marriage: people are pretty adept at complaining about a miserable partner – but what they seldom recall is why they got married in the first place.
http://www.star2.com/food/food-news/2016/05/22/a-fat-lot-of-good-part-3/http://healthticket.blogspot.my/2016/05/a-fat-lot-of-good-part-2.html
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