Making body fat, without eating it

Carbohydrates dominate our food landscape and are endorsed by current dietary guidelines that recommend getting something like three-quarters of our calories from them. Carbohydrates are built with molecules of glucose, and from the perspective of our metabolism, they are simply a source of glucose, including glucose from starch (rice, wheat, tubers, legumes), sugar (white sugar, brown sugar, high-fructose corn syrup, honey), and most fruits. Fruits are sugar and water. For example, grapes are 97% sugar and water, apples 95%. These are not health foods.

While we are not encouraged to eat refined sugars, we are encouraged to eat fruits and starchy carbohydrates (including refined carbohydrates because they are fortified, and a high-carbohydrate diet without them is nutrient deficient). Most people would eat sugar as well. With this landscape, it is easy to overload our bodies with glucose beyond our energy needs on a daily basis.

What to do with this surplus glucose? Evolution solved that a long time ago – make fat out of it. There’s an irony here – we are discouraged from eating fat in our high-carbohydrate dietary guidelines, but silently our bodies are making it anyway. This is why a high-carbohydrate low-fat diet can be fattening. Indeed, when other mammals like grizzly bears need to accumulate fat for hibernation, they seek out fruits, berries and other carbohydrates. They don’t seek out fat. Bears understand intuitively that eating fat is not the best way to get fat.

1. What is body fat?

Biologically, what we call fats are triglycerides (TGs) – molecules made up of three fatty acids (FAs) attached to a glycerol molecule. Think of a TG like the letter E, the vertical line of the E is the glycerol molecule, and the three horizontal lines are the three FAs (but longer than that, and not necessarily straight).

FAs are a chain of carbon atoms of varying lengths (with hydrogens attached). The FAs I will mainly refer to are long-chain (~16-22 carbon) FAs. They can be straight (saturated) or bent in various places (unsaturated). If there is only one bend, it is a mono-unsaturated FA. Multiple bends and it is poly-unsaturated. Different types of FAs can be incorporated into a TG.

The glycerol backbone of a TG can be synthesised from glucose, and readily converted back to glucose. Thus, TGs package our two principal biological fuels: glucose (as glycerol) and FA.

2. The FA profile in fat

The three FAs that predominate in the fat of mammals that form part of our diet are: palmitic acid; stearic acid and; oleic acid (although there are many others in much smaller amounts). The first two are saturated, while the third is mono-unsaturated. The proportions of these FAs are roughly the same across species. Something like 30% saturated (palmitic + stearic) and 50% mono-unsaturated (oleic). Hence, mammal fats are predominantly mono-unsaturated oleic acid, despite their reputation as saturated fats. Furthermore, oleic acid is the main FA in olive oil.

All of this applies to our own fat as well – it is ~30% saturated (palmitic + stearic) and ~50% monounsaturated (oleic). That shouldn’t come as a surprise, as mammals evolved together and the mechanisms for fat storage, synthesis and trafficking were laid down a long time ago in our common evolutionary development.

These simple observations highlight another dietary folly – to restrict dietary fat from land-animals when our own body fat has the same FA profile as theirs. Evolution would have selected this FA profile for a reason, and we would be better advised to follow it, not deny it, in our diet.

3. The ‘essential’ FAs

There are two forms of FA that we need to get from our diet (known as ‘essential’ FAs), the rest we can synthesise ourselves. These are the omega-6 and omega-3 forms of FA (there are about 10 FA types in each form). Even then, it is not that we can’t synthesise them at all, but rather that the rate of synthesis is very slow and it is more practical to get them from the diet. They are all poly-unsaturated FAs, with more than one bend in the carbon chain, the last one being 6 or 3 carbon atoms from the end (hence the naming convention, omega being the end letter of the Greek alphabet).

As these are ‘essential’, our bodies will maintain a store of them in adipose tissue if there is a dietary excess. Unfortunately, our diet is very excessive in omega-6 and deficient in omega-3

I have seen levels of up to 10% reported for omega-6 in our adipose tissue, while omega-3 was barely detectable. This is alarming because omega-6 is pro-inflammatory. It would normally be balanced in our body by omega-3, which is anti-inflammatory. The imbalance reflects our diet which is high in sources of omega-6, such as refined poly-unsaturated ‘vegetable’ oil, and low in omega-3. This can contribute to chronic inflammation, which is a precursor for many modern disorders (ironically, including heart disease).

4. Using fat

We need fat for our biology to function. For example, we need FAs to form the membranes of all of the cells in our body (I am not aware of any exception). FAs are also signalling molecules and have roles in gene transcription and regulation. FAs are also an energy source, can fuel skeletal muscle, and are the primary fuel for the heart. The healthy heart has little use for glucose (although it can metabolise any fuel in an emergency). Unlike skeletal muscle, the heart does not keep a glucose (glycogen) store. In fact, it has no fuel stores of significance and relies on a constant supply of FAs from the circulation in real-time. If there is an interruption to fuel supply, the heart has only enough energy available to sustain it for 10 more beats.

The irony is that dietary guidelines urged us to limit fat in the diet, to be heart-healthy, whereas FAs from fat are what the healthy heart needs to keep beating – around 100,000 times a day.

5. Making fat

When the low-fat diet was first proposed, decades ago, there was genuine alarm from scientists that it could be dangerous for the heart and our biology. Fortunately, if the diet is deficient in FAs, most cells in our bodies can synthesise them from glucose. Still, the liver is the primary factory for synthesising FAs.

Liver cells start with glucose (which has 6 carbon atoms per molecule) and break it down into three molecules with two carbons apiece. These molecules are acetates (related to the acetic acid in vinegar). In a multi-step process, these acetates get joined end-end to form longer carbon chains (always with an even number of carbons). The first landing in this process is when the chain gets to 16 carbons long – some oxygens and hydrogens are added at each end, and we have our first significant FA from glucose – palmitic acid. It is a small step to add another two carbons, yielding stearic acid. The carbons were added in a way that makes both of these FA saturated. In a further step, the stearic acid is given a bend 9 carbons from the end, making it a mono-unsaturated omega-9 FA – this is oleic acid.

We now have all three of the major FAs that we, and other mammals, store in adipose tissue. To form a TG from them, glycerol is synthesised from glucose and three FAs attached. The TG can then be ferried, from the liver to adipose stores, in structures known as lipoproteins. The process of moving TGs (and other fat-like molecules such as cholesterol) around our water-based body is interesting, but too large a topic for this post.

The process of storing TGs in cells of adipose tissue (adipocytes) involves breaking down the TG into its FAs and glycerol on the cell surface, transporting these across the cell membrane, then reassembling the TG on the other side.

The liver has started with dietary glucose, but stored fat. Furthermore, the conversion of glucose to FA and then TG is accelerated in the presence of insulin, which is released by the pancreas in the presence of high dietary carbohydrates. This pathway is further accelerated in the presence of insulin resistance.

If there is too much TG generated in this way by the liver, because of carbohydrate-overload, or if the liver cannot synthesise the lipoprotein carriers fast enough to meet demand, the TG can accumulate in the liver and ultimately give rise to non-alcoholic fatty liver disease (NAFLD). NAFLD is on track to become the most common cause of liver disease in Western countries. Its prevalence is estimated to be ~20-30% of the adult population (90% in obese individuals, 50% in those with type 2 diabetes). NAFLD associates with Metabolic Syndrome (diagnosed if 3 of the following apply: obesity; high blood pressure; high blood glucose; high TG; reduced high-density lipoprotein (HDL)). Metabolic Syndrome in turn associates with increased risk of developing heart disease and type 2 diabetes. While these are only associations, there are some who suggest that NAFLD is the precursor to these, and other, non-communicable diseases of modern living (including cancer and Alzheimer’s disease) – it starts with insulin resistance in the liver.

6. Dietary fibre

It is not only digestible carbohydrate that can get turned into FAs, dietary fibre from carbohydrate can be too. Our multitude of bacteria in the colon ferment fibre for their energy needs. The ‘waste’ products are FAs, gasses (such as carbon dioxide, methane) and water.

In this case, the FAs have only short carbon chains (5 or less) and are thus referred to as short-chain FAs. Two examples are butyrate (4 carbons), and acetate (2 carbons). Butyrate is an important fuel source for cells of the colon wall, and the liver metabolises the remainder. Acetate can be used for energy in multiple organs, or join in with the synthesis of long-chain FAs in the liver.

While digestible carbohydrates will be used to synthesise FAs if consumed in excess, resistant carbohydrates (such as fibre) will result in absorption of FAs at all levels of consumption.

7. Dietary fat

What happens if the diet has a surplus of FAs from fat, such as vegetable oil, that does not contain FAs in our preferred forms (palmitic, stearic, oleic)? The FAs can be broken down into their acetate building blocks, and re-assembled to synthesise our preferred FAs. You’re not what you eat.

8. Dietary protein

Our other macronutrient – protein, can also be used to synthesise fat. We have no way to store protein unless we are experiencing muscle hypertrophy. While we can burn the amino acids in protein for energy, or use them to synthesise other biologically-important molecules (e.g. enzymes, hormones or neurotransmitters), any excess protein must be managed. Most of the 20 amino acids that make up protein can be converted to glucose (a few can be converted to ketones, and some into either glucose or ketones). A main (but not only) difference in the composition of glucose and the amino acids is nitrogen. This gets removed and excreted in urine as an ammonia-like molecule. What remains is fashioned into glucose. The glucose can then be utilised for energy, or made into fat as just described. It is for this reason that a low-carbohydrate ketogenic diet should not be high in protein – the calories need to come from fat instead.

9. Ketosis

In ketosis, the body is adapted to burning FAs for fuel. If these are coming from TGs in adipose tissue stores, the TGs are first broken down to release their FAs and glycerol, which are transported out of the adipose cells. The FAs are attached to a large protein called albumin, which enables them to travel around the blood circulation. The glycerols are water-soluble and travel on their own. Powerful regulatory mechanisms, that are still not fully understood, continually match the FA released to FA demand. The FA is used to fuel skeletal and heart muscle. Extra FA is broken down in the liver to ketones that the liver itself cannot use for fuel. Instead, the ketones are released into the circulation and readily cross the blood-brain barrier to fuel brain cells. They can also fuel the heart. The liver synthesises glucose from glycerol according to demand.

Our evolutionary machinery is humming.


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Related Posts:

Main ketogenic diet page.

The problem with fruit.

Reasons not to eat refined ‘vegetable‘ oils

A different (hormonal) model of obesity.

The failed workings of dietary committees on fat

Our heritage fats

Further detail on a ketogenic diet.