Why Did the Chicken Cross the Road?

Phil Nuttridge continues his series of articles looking at the modern take on diet and nutrition.  He explodes many of the dietary myths that defined the latter decades of the twentieth century and left their legacy of chronic illnesses in the first decades of this century.  In this month’s article he looks at vegetable seed oils and the polyunsaturated fats they contain and how they are linked to insulin resistance and chronic illness.  More information can be found on Phil’s website http://cuttingcarbs.co.uk or by following him on Instagram:  CuttingCarbsUK

Question:  Why did the chicken cross the road?

Answer:  To avoid being confused with margarine.

Let me explain.

Having had the privilege of being one of the contributing authors for Jane Sheehan’s recently published “Gurus’ guide to Reflexology:  Volume 1”  [ https://footreading.com/product/the-gurus-guide-to-reflexology-book-1/ ] I have been invited to contribute to her upcoming third Gurus’ guide which will be focussing on cancer.  My research for that up-coming contribution – I will be writing the chapter on nutrition and cancer – has already led to some very interesting insights.  Spoiler alert: beware the ‘not-so-healthy’ seed oils and margarines.  Whilst you will have to wait for the third Gurus’ guide for the full explanation (and biochemical science) of how these manufactured food-like substances lead to cancer, what I am excited to share with you now is some very up-to-the-minute research which neatly explains one of the nuances of insulin resistance discussed in previous articles in this series.  

It’s not just carbs that lead to insulin resistance; it could be the mayonnaise, the salad dressing, the dairy-free spread you are eating.  It could even be the chicken, bacon and eggs on your plate!

INSULIN 101

Let me re-cap first.  Insulin is the hormone your pancreas releases to lower blood sugar levels whenever they rise above safe limits. If you have eaten a meal high in digestible carbohydrates (cakes, biscuits, bread, pasta, rice, root vegetables, fruit, fruit juices for example) then the sugars released from that digestion will enter your blood circulation.  This will raise your blood sugar level.  Whilst we can burn sugar for energy it is not our only source of energy and indeed evolutionarily it is not our primary energy source – that accolade goes to fats.  In fact, too much sugar in your blood for too long is not good and so we have evolved sophisticated systems to use-up or squirrel away excess sugar from circulation.  The chief weapon in this defence against sugar is the hormone insulin, released by the pancreas and sending a message around the body to get on and deal with this surge of digested carbs.

So what does insulin do?

  • Insulin signals to the liver to stop making sugar (this is something the liver can do obviating the need for carbohydrates in the diet) and instead instructs the liver to make a starch called glycogen from the excess sugar.  Glycogen is a ‘reserve’ that gets sugar out of circulation but leaves it in a form that is readily available for later use.  Once the liver is replete with glycogen, it will then convert further excess sugar into fats ready for storage either around the internal organs (visceral fat) or under the skin (subcutaneous fat).  Excess of either of these fat reserves is bad news.
  • Insulin tells the muscles to stock-up on their glycogen reserves too by triggering the muscle cells to enter ‘anabolic’ mode.  This same metabolic mode also triggers protein synthesis allowing muscles to repair and build.
  • Insulin instructs all cells of the body to enter ‘sugar burning mode’ and make sugar temporarily their primary fuel for energy release.  Insulin also blocks a number of pathways needed for ‘fat burning mode’ yet further encouraging sugar burning.
  • In the fat cells in your skin (adipocytes), the insulin instruction causes changes that demote fat breakdown and promote sugar uptake and fat building.  The insulin message tells adipocytes to stop breaking down and releasing its fat reserves into the blood (lipolysis) and instead triggers the cell to take-up fats and excess sugar from the blood and convert those to storage fat (lipogenesis).  In other words, insulin tells the adipocyte cells to get fatter.

If you have a diet that is regularly high in carbohydrates, you start to put this insulin system under strain.  As this happens, the cells that should be listening to the message become a little deaf to its signal.  So the pancreas has to release more insulin to get its message across.  But this deafness begets more deafness requiring the pancreas to release yet more insulin.  This is what we call insulin resistance.  In extremum, the pancreas cannot release enough insulin to get the message sufficiently heard and this is Type II diabetes.

However, the problem with insulin resistance is multi-faceted.  It has been observed that different parts of the body become insulin resistant at different rates.  For example, if the liver becomes ‘deaf’ quite quickly but the skin fat cells do not, then this triggers obesity.  In this scenario, the liver still churns our glucose because it hasn’t heard insulin’s signal to stop but the skin cells’ lack of insulin deafness means every single part of the message to ‘store fat, store fat, store fat’ gets heard and actioned.

What has remained elusive is a metabolic understanding as to why some tissues become insulin resistant more readily than others.  Why should the liver become deaf to insulin sooner than the skin cells?  Is it genetic?  Is it based on a lifetime of dietary choices?  Is it environmental?  In part it is ‘yes’ to all of those, but exciting new research is suggesting that there is a very strong and consistent trigger coming from refined seed oils.  

To explain this I need to give you a little primer on fats and oils in your diet.

FATS 101

There are principally two sorts of fats in your diet – saturated and unsaturated.  This is a biochemical distinction: Saturated fats have a chemical structure where all possible chemical bonds have been fully filled; unsaturated fats have a bit of room left for (usually) hydrogen to be added.  

This lack of saturation in these unsaturated fats has four consequences:

  • The molecules in unsaturated fats cannot pack as tightly together as the molecules in saturated fats because the not-fully-filled bonds produce a ‘kink’ in the unsaturated fat molecules.  Fats high in unsaturated molecules tend therefore to be liquid at room temperature; saturated fats tend to be solid as the straighter unkinked molecules can pack hard against each other.  This has health implications as it means the unsaturated oils have to be chemically manipulated to make them solid at room temperature: Beware those vegetable/seed based margarines!
  • The unsaturated bonds (the bonds that could take more hydrogen) are chemically unstable.  Thus oils made from unsaturated fats are more likely to go rancid and oxidise.  This has huge implications for the storage and shelf-life of these oils but more importantly once consumed, this instability and readiness to oxidise makes them very harmful to metabolic health.  I shall leave the full discussion of this and its role in cancer formation to third Gurus’ guide.
  • Not all unsaturated oils are bad though.  Some ‘mono’ unsaturated fats (like those predominantly in olive oil) have only one bond that is not fully filled.  These are much more stable than oils which have multiple non-fully-filled bonds – known as ‘poly’ unsaturated oils.
  • The presence of multiple points were extra hydrogen could be added, make the processing of polyunsaturated fats for energy in the body very different from that for saturated fats.   It is this last point that is now being linked to insulin resistance.

Saturated fats are found in foods we have eaten for most of human history – coconut oil, lard, butter, meat fat and dairy.  Yet these fats have been demonised over the last 60 years as the cause of heart disease.  This is something I have discussed previously in this series of articles and have now also explored in my nutrition lecture series  (http://www.cuttingcarbs.co.uk/survival-of-the-fattest/).  I assure you the only way saturated fat could ‘clog’ your arteries is if you intravenously injected it!

Polyunsaturated fats (PUFAs) occur in oily fish (known as the omega 3 fatty acids) and seed oils (predominantly the omega 6 fatty acids).  Whilst both are essential to our wellbeing, beware too much omega 6 in your diet.  Moreover, omega 6 fats rarely exist in nature in their free state and yet in the last 60 years we have chemically extracted them from seeds to produce the oils that we now cook with, drizzle over our salads and (most critically) add to processed foods.  These oils are cheaper than the naturally occurring mono-unsaturated and saturated fats and, in the paradigm that saturated fat is bad for you, the PUFAs have (wrongly) been idolised as the healthy alternative.   But they are unstable, readily oxidised, chemically extracted and manipulated (bleached and deodorised), often processed to make them solid at room temperature (for margarines and ‘shortening’) and disturb our metabolism causing inflammation and auto-immune responses. 

I am going to run with that last point. 

This will necessitate some biochemical details – if you would rather skip that bit, you can jump to the heading ‘THE KEY POINT’!

FAT METABOLISM 101

When you consume fats, our bodies have to chemically engage with those molecules making them more readily usable in metabolism.  One of the key processes, and please forgive me for the next few paragraphs will get quite technical, is known as β-oxidation.  This breakdown process for long chain fats takes place inside the energy power plants in our cells known as mitochondria.

β-oxidation essentially chops off the end bit of the long chain fat molecule and makes the snipped-off piece into Acetyl-CoA which can then fuel the energy releasing processes in the mitochondrion.   What is left of the fat molecule, now a little bit shorter, is fed back into β-oxidation for the process to happen again.  This cycle is repeated until all the useful parts of the fat molecule have been snipped-off.  This is summarised in the diagram below: 

Notice two other by-products of the process:  NADH+H+ and FADH2

This is where your body feels the difference between a saturated fat and a polyunsaturated fat:

  • If you put a saturated fat through β-oxidation, the ratio of FADH2 to NADH+H+  is higher.
  • Put a polyunsaturated fat (PUFA) through β-oxidation, the ratio of FADH2 to NADH+H+ is lower.

This difference is key to the fat storage cells in your skin, known as your adipocytes.  Adipocytes have an elegantly evolved response to saturated fats, a measure of how long these fats have been a natural part of our diet.  Evolution and our adipocytes however have not had long enough to develop a healthy response to the raised levels of PUFAs in our modern diet.

When you eat saturated fats, our evolved response to the higher FADH2 to NADH+H+ ratio triggers the adipocytes to become insulin resistant. Yes, I did just say that eating fats we have eaten for most of human history makes our skin fat cells insulin resistant.  But as I am about to show, this is a good thing!

You might remember from earlier that insulin tells the adipocytes to get fatter.  And if your adipocytes get fatter, you get fatter.  Recall that this happens because insulin switches off the process of releasing fats from the adipocytes and switches on the process where adipocytes take-up fat and glucose from the blood.  Just as a bank account swells if more money comes-in than goes out, so too fat cells swell when there is an insulin-triggered net uptake of fat.

If you eat lots of saturated fats, you make your adipocytes insulin resistant (the higher FADH2 to NADH+H+ ratio signals the mitochondria to down-regulate the insulin receptors in the cell) and they ignore the message to be thrifty.  Instead they release lots of their fat reserves as fatty acids into the blood (the bank account gets smaller).  These free fatty acids in circulation provide an energy-rich and low inflammatory fuel for the cells in your muscles, brain and liver.  Keeping your adipocytes insulin resistant stops them from becoming fatter so you don’t become fatter.  Eating saturated fat is a win-win for your fat cells and your body cells.

If however you get the FADH2 to NADH+H+ ratio the wrong way round by eating lots of PUFAs then your fat cells stay insulin sensitive (the insulin receptors are still switched on to full capacity).  The adipocytes keep hold of their fat reserves and keep adding to them.  They get fatter and so do you.  And what’s more the vital cells in your brain, liver and muscles are not now supplied with the energy dense fatty acids (that would be released from insulin resistant fat cells) and so crave extra insulin to get more sugar into their own cellular metabolisms.  Those brain, liver and muscle cells therefore become insulin resistant.  Insulin resistance in your skin fat cells is good; it is not good for the rest of your body.

PUFAs also affect the insulin sensitive adipocytes in another way – they inhibit the formation of new fat cells.  Instead of new cells taking a share of this increasing fat storage burden, the existing adipocytes have to take it all.  They become overburdened with fat.  In many cases this triggers inflammation and an auto-immune response as the over-sized fat cells release distress triggers that stimulate the immune system into action.  Cue inflammatory and auto-immune diseases.

THE KEY POINT

A diet high in PUFAs (polyunsaturated fats) keeps your fat cells insulin sensitive yet triggers the rest of your body cells to be insulin resistant.  This creates the perfect storm for obesity, inflammatory disease, auto-immune disease, cancer and type II diabetes.

“Do I eat polyunsaturated fat?” is probably then the question racing through your head right now.  The main polyunsaturated fat you need to be worry about is linoleic acid.  This is one of those omega 6 fats I warned about earlier and it is the most highly consumed of the PUFAs.

The first food source I want you to cross off your list is margarine.  All margarines.  Not only are they full of linoleic acid they have been chemically manipulated to make them solid at room temperature.  Please, if you have margarine in your fridge, destroy it right now.  I am not normally one who is comfortable with food waste, but as margarine is not a food, destroying it is a public service rather than a waste.

The next food source to consider is the ‘vegetable oils’.  Firstly this is a misnomer: They are not extracted from vegetables as we know them – not broccoli, nor cauliflower nor cabbage – but from seeds, beans and legumes:  Rapeseed oil, sunflower seed oil, soybean oil, peanut oil (peanuts are neither peas nor nuts – they are legumes), grape seed oil, corn oil, cottonseed oil.  If you have any of these in your cupboards, destroy them.  Again that is a public service and not waste.

But here is a bigger problem.  You might not have tubs or bottles of these in your cupboard but every time you buy a salad dressing, a mayonnaise, a dip, a pre-made sauce, fast food or a takeaway they are likely to be full of them.   So too will be a supermarket-sourced cake, biscuit, packet of crisps, loaf of bread, ready meal, dried fruit, muesli or a vegan alternative to a meat-based food. They are cheap to produce and much cheaper than naturally sourced saturated fats.  But profit margins are not health margins.  

For example, most mayonnaise is made with rapeseed oil (high in linoleic acid).  To have a mayonnaise without PUFAs then, you need to either make your own or buy from specialist websites.  [Beware certain branded mayos that claim to be made with ‘extra virgin olive oil’ – yes they may have olive oil in them, but their main oil is still rapeseed].  And then think of how often you eat PUFA-laden mayo:  Coleslaw as a side dish in a restaurant, a bought prawn cocktail, that party-dip selection pack, that sandwich you had for lunch (and remember it is probably in the bread too) and that tuna mayonnaise you had in your jacket potato.  

Even restaurants and delicatessens could be using them under the misguided belief that they are healthier than saturated fats.  Fried food is almost invariably cooked in them – this is disastrous as remember PUFAs are unstable and liable to oxidise and especially under heat.

You do need some linoleic acid in your diet.  So a few sunflower seeds are useful.  The PUFAs in the whole seeds have not been chemically extracted and manipulated, as they are in there ‘raw’ state they are stable and are combined with lots of other useful nutrients in the seed.  Never though consume sunflower seed oil.

It is estimated that the healthful ratio of omega 6 fats to omega 3 fats is around two to one.  Because of the prevalence of seed oils in our diet and therefore the hidden consumption of linoleic acid, it is estimated that for many people the consumed ratio is around 20 to 1.  Those who consume a lot of processed and convenience food will have a still higher ratio.  Is it any wonder therefore that there has been a sharp rise in obesity, diabetes, auto immune and inflammatory diseases over the last decades where we have been told to replace saturated fats with ‘healthy’ polyunsaturated fats?  Add to that our insatiable appetite for refined carbs and we have the perfect storm of ill health.

WHY DID THE CHICKEN LOOK LIKE MARGARINE?

The title of this piece asked why the chicken crossed the road.  I have some bad news if you think chicken is always a healthier alternative to red meat.   

You have probably heard the phrase “you are what you eat”.  Well let me expand that: “You are what you eat has eaten”.  Chickens would naturally eat wild green plants, wild seeds and animal foods such as earthworms and insects.  If the chicken you eat (or its eggs) has eaten those things, chicken is a great food and deserves a prominent place in your diet.  However, to fatten chicken and raise them as quickly and cheaply as possible in a competitive food market, they are often fed corn and soya beans instead.  Neither of these ‘foods’ are natural for a chicken.  The PUFAs in the soya and corn become incorporated in the adipose fat of the chicken: If you eat that chicken you consume those PUFAs.

I am afraid the same is true of pork.  Pigs naturally would have a diet not too dissimilar to wild chicken – grasses, roots, small animals and insects.  Pork raised in this way is very healthful.  However, all to often battery raised pork is fed corn and soya and yes, you have probably guessed already, eating pork products of those animals will also increase your PUFA intake.  Not all bacon is made the same!

Ruminants on the other hand have an enzyme that allows the linoleic acid to be converted to less harmful unsaturated fats.  Whilst I would consider it indefensible to raise ruminants on anything other than grass (they are a essential part of the topsoil cycle), if you do eat beef and lamb raised on soya and corn at least you are not adding significantly to your harmful PUFA intake.

The same dietary guidelines that told us to eat more vegetable oils (wrongly) and reduce our saturated fat intake (wrongly) also told us to eat eat more poultry in preference to red meat.  On all of these targets we have done what we were told (saturated fat consumption down, vegetable oil up, poultry up, red meat down).  But, the economic pressure to produce more poultry more cheaply has put corn and soya fed chicken into the food chain, adding to disease-causing PUFAs in our diet.

So what is the take home?  Get as many sources of polyunsaturated fats out of your diet as possible. No margarines and no ‘vegetable’ oil (let’s call them by their proper name – refined seed oils).  Be a more discerning shopper when it comes to packet, tinned and bottled food:  Look at the label and avoid foods with the refined seed oils.  

Be a canny meat shopper too.  Ask your butcher what the chicken and pigs were fed on.  The more natural their diet, the more healthful they will be to you.  And although beef and lamb are less likely to contain PUFAs even if raised on a poor diet of corn and soya, pay the extra to have grass-fed.  

And to replace the PUFAs stored in your adipocytes (from all those years of following the advice to eat ‘healthy’ vegetable – a.k.a refined seed – oils) up your intake of saturated fat.  Cook with lard, beef suet, goose fat and coconut oil; eat fatty cuts of properly fed meat; eat beef suet; eat dairy from responsibly raised herds.  Eat as your ancestors would have eaten – that is what your metabolism is evolved to expect!