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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 supplements and shares some thoughts on why it might be beneficial to take them.  More information can be found on Phil’s website cuttingcarbs.co.uk or by following him on Instagram:  CuttingCarbsUK

He took a bottle from his pocket and shook from it a tablet about the size of one of his fingernails.

“That” he announced “is a square meal in a condensed form.……..It contains soup, fish, roast meat, salad, apple dumplings, ice cream and chocolate drops, all boiled down to this small size, so it can be conveniently carried and swallowed when you are hungry and need a square meal”

From The Patchwork Girl of Oz

Eating pills instead of food was the stuff of science fiction when I was a boy.  You could not boldly go anywhere in the Universe without your nutritious pills.  Today, if you survey the shelves of supplement pills in any health-food store or supermarket you might be forgiven for thinking that day is virtually upon us.  But what of the reality of supplement pills?  Does a pill a day (or indeed, multiple pills a day) keep the ailments away?

Firstly, let me pin-down the chemicals those supplement pills are offering us.  In a very simplistic model there are two key components of our diet: Macro-nutrients and micro-nutrients.  The macro-nutrients are the carbohydrates, fats and proteins that should form the bulk part of the food you eat; fats and proteins are essential macro-nutrients and must be part of your diet.  Whilst we do not normally consider any of these as worthy of supplementation, some people do.  Body builders for example use protein supplements to (supposedly) enhance muscle repair and many of us take fish oil (fat) supplements to boost the essential omega 3 fatty acids.

Micro-nutrients are then the chemicals needed by your body but in much smaller quantities.  Traditionally this group is sub-divided into vitamins and ‘minerals’ although as you will see I will use the more accurate label ‘essential elements’ for this latter group.  In all there are thirteen identified vitamins, each of them an organic compound vital for the body to function – A, D, E and K are the fat soluble vitamins; the B group and vitamin C are the water soluble ones.  Some vitamins can be made in the body (for example vitamin D can be synthesised in the skin from sunlight and cholesterol) but for most people, these thirteen vitamins need to be part of the diet either through food or supplements.

Macronutrients and vitamins give our bodies the elements of carbon, hydrogen, oxygen and nitrogen. In addition there are other elements essential for body function: Calcium, sodium, potassium, magnesium and phosphorous are the primary essential elements; iron, zinc, manganese, copper, molybdenum, iodine, chromium and selenium are further elements needed by the body but in much smaller ‘trace’ amounts.  Traditionally this would all be grouped as the ‘minerals’ but in the strict chemical definition of this term, not all the elements listed above are actually minerals.  These essential elements and trace elements, like vitamins, have to be part of our diets either through food or supplements.

When we think of supplements we are usually referring to these vitamins and essential elements.  Additionally, there are a number of supplements that people might take that do not neatly fit into this classification.  

Examples of these ‘other’ supplements are:

My primary focus in this article will be the vitamin and essential element supplements but I will touch on some of these other supplements as part of that journey too.  I shall devote an entire article (entitled ‘Not a fibre of truth’) to fibre, as that is a very interesting story in its own right. 

OK, so we have now met the key players in this story of supplements.  But let us step back a moment: Human physiology has little changed over the millions of years that hominids have been around.  We have survived without pills for most of that time so why on Earth would we need them now? 

That is a good question but one I can very easily deflect.  Essentially, we have lost our way with nutrition:  We no longer eat what we used to and we no longer eat in the way we used to.  And although some of the foods we eat today may resemble what we might have eaten in our distant past, those foods are but a shadow of what they used to be in terms of their nutrient content.

Did you know, for example, that strawberries from fifty years ago are estimated to have had twice the vitamin C content of modern-day strawberries.  Supermarket-bought strawberries, forced to grow out of season, hybridised for their sweetness (rather than their nutrient content), shipped half way around the world and sprayed to keep their appearance, have even less.  

When we were ‘gatherers’ (as part of our hunter-gatherer past) the things we scavenged were predominantly leafy green vegetables – fruits were rare and very seasonal in our bleak northern European habitat of old.  When meat was scarce, it is hypothesised that we probably gathered over 170 different species of leafy green vegetable to ‘supplement’ our diet.  Nowadays we eat fewer than twenty species of leaves.   And as with the fate of modern strawberries, the leaves we do still eat are excessively hybridised, grown out of season and on poorly nourished soils, all factors that deplete their nutrient content compared to varieties in our ancient past.  

Our modern-day sweet tooth also means we are drawn to the wrong sorts of vegetables – the starchy root, grain and cereal crops all of which bring lots of carbs and calories to the table but alas very few of those essential nutrients we need.

When it comes to meat, things fare little better.  Because we have been led down the wrong path of ‘fat is bad’, most modern cuts of meat we now eat lack the marbling of fat that brings flavour but more importantly brings the fat soluble vitamins A, D, E and K.   The pressure to produce cheap food has led to some very unhealthy practices regarding the way we raise meat.  Ruminants fed on soy, grains and cereals are not only harmful to the environment but also their meat contains far fewer nutrients (for example) omega 3 fatty acids than ruminant-meat raised on grass as Nature intended.  We also now shun the organ meats and yet these were staples for our parents and grandparents.  Did you know liver is the most micro-nutrient dense food there is?  Bar none.  It even contains vitamin C and in a form that is more heat stable than in fruit. 

So as you can see we have rather lost our way with regard the food we eat and its nutrient content.   You will often hear people say “If you have a balanced, healthy diet then you do not need to take supplements”.  In an absolute sense that would be true if we all did indeed have a nutritionally fulfilling human diet, but most people’s diets nowadays are neither balanced nor healthy.  We have disconnected from the foods that made us human.

For me there are five circumstances when you should consider taking supplements.  You should think seriously about supplementation if:

I shall look at each of these circumstances in a little more detail.  Lest you think that I am nothing more than a pill-pusher, at the end of this article I shall show you how by incorporating a few traditional foods into our diet (actually, put them back in our diet) we can get many of the missing nutrients once more onto our plates without recourse to pills.  Not everything needs to be solved by taking a pill.

1. You rely on supermarkets for your food.

As I have already described, the nutrient load of many of the foods we eat nowadays is far less than it used to be.  Intense mono-crop agriculture that depletes soil resources, the need for new hybrids of crops for fast growing, disease resistance, enhanced flavour and longer shelf-life are all to the detriment of the level of nutrients contained within those foods.   Plant foods are grown for profit margin, not the goodness they deliver.

Yes, if you grow your own vegetables with good soil management, then you can overcome much of this.  If you insist on meat with good provenance, organically raised and grass fed, then you will have highly nutritious meat.  But if you can only source your vegetables and meat from supermarkets, then you may well find yourself low on certain key nutrients making supplementation beneficial. 

The tendency of many to over-eat is probably in part due of this diminished nutrient density of your food.  Our bodies are innately programmed to seek nutrition – the vitamins and essential elements needed by our bodies.  But if the food we eat is not providing enough of these key nutrients, then the body will continually make us feel hungry encouraging us to seek more food to supply that shortfall in nutrients.  You will want to eat twice as many modern-day strawberries to get all that vitamin C you need.  Whilst that over-eating may well top-up the missing nutrients, it will over-load our bodies with surplus calories and in the case of those strawberries, too much of public enemy number one:  Sugar.  Our desire to over-eat can therefore be a measure of our programmed need for nutrients being poorly met by supermarket-bought food.   Never before have we been so over-fed yet under-nourished!

2.  You are on a restriction diet

Our omnivorous evolution means that we have metabolic adaptations to eating both animal products and some plant products.  But the key thing about being an omnivore is that we should eat both animal and plant foods.  

There is a somewhat disturbing plant-based fad at the moment, its followers cutting all meat products from their diet on the basis of health and for the environment.  Whilst my analysis of how properly raised meat is in fact good for the environment is beyond the scope of this article, allow me to dispel a few myths regarding a meat-free diet and good nutrition. 

We will often hear how “carrots are full of vitamin A”, or “mushrooms (left out in the sun) are full of vitamin D” or “spinach is full or iron”.  Alas, this is misleading.  Yes, in the laboratory, that vitamin A, vitamin D and iron can be extracted into a test tube from those plant foods. Unfortunately our human bodies cannot do the same.  The vitamin A that humans need is in the form of retinol but the form in carrots is carotene.  Many of us cannot process carotene and even those of us who can are only able to access a meagre proportion of it.  Meat, particularly liver, contains retinol aplenty.  You would have to be continually munching on many kilograms of carrots to get the vitamin A load of just 100g of calves’ liver.  

To get the recommended daily dose of vitamin D you would need to eat 3kg of mushrooms every day but even then it would be in a form called D2; humans need the D3 form.  Just one teaspoon of cod liver oil would give you three and a half times your daily requirement of this vitamin and in the right form.  All that mushroom munching would be in vain.  

The iron in spinach is a form termed non-haem; humans however need the haem form found in red meat.  I assure you, Popeye did not get his muscles from eating spinach.  

So if you are choosing to eliminate animal products from your diet, the list of vitamins and essential elements you will be deficient in, and should therefore consider supplementing, include:

3. You are on prescribed medication.

Most prescribed medications have side-effects.  Some of these side effects are little more than inconvenient but some are rather more serious.  In a number of cases, an appropriate intake of supplements can mitigate some of these side-effects.  For example, statins are a drug prescribed to lower cholesterol  although you should read my previous article if you are under any illusion that this is a good idea.  The way statins do this is to interfere with the chemical pathway in the liver that produces cholesterol. Unfortunately, this same chemical pathway also produces other useful chemicals for the body, one of those being co-enzyme Q10.  Statins interfere with the body’s ability to make this vital chemical and so supplementation with CoQ10 is essential for those taking statins.

4.  You have a diet high in ‘anti-nutrients’.

The subject of ‘anti-nutrients’ is a growing area in nutrition research and one I shall address in a future article (entitled: “Vegetables ARE out to get you”).  Essentially plants do not want to be eaten – who does – but unlike animals they cannot fight or run away.  Instead plants engage in chemical warfare.  A whole range of ‘anti-nutrients’ have developed in the leaves, husks and fruits of plants that intentionally harm any animal or insect that may eat them, making the plants less likely to be eaten again.  For example, soy and flax contain phyto-oestrogens whose main evolved purpose seems to be to make insects that eat them sterile.  A perfect strategy if you want to avoid being eaten by insects!

Research is showing that plants have evolved a myriad of chemicals with the same end objective of reducing their chances of being eaten.  Many of these chemicals are in the plants we humans eat.  For example, if you eat a diet high in spinach, kale, asparagus and rhubarb you will expose yourself to oxalates.  These chemicals interfere with your calcium metabolism, producing crystals in the body where they should not be, for example in the joints (gout), in the kidney (kidney stones) or in the gall bladder (bile stones).  Supplementing with magnesiums citrate can mitigate some of these effects as can taking calcium supplements.  This latter strategy does not necessitate taking pills as you could of course just make sure you have a good source of calcium in the same meal as the oxalate containing vegetables: Have some feta with your spinach, have some cream with your rhubarb!

5.  You are seeking a health outcome that can be improved with high dosage of key micronutrients.

Vitamin C is a great way to battle colds.  Some nutritional therapists advocate up to 1000mg of Vitamin C every hour at the first onset of symptoms to help your body battle the cold lurgy.  Yes, you read that correctly – 1000mg every hour.  (You stop taking the hourly dose of vitamin C once the symptoms subside or you start running to the toilet, a sign that your body no longer needs the excess vitamin).  This is way above the recommended daily intake of vitamin C of just a few hundred milligrams per day but that recommendation is merely enough to stop you getting scurvy.  The high dosage being advocated here is that to achieve a significant ‘other’ health outcome. 

There is no way you could consume enough fruit to achieve 1000mg of Vitamin C every hour and nor would I recommend it even if you could, as that much fruit would over-load your body with sugar and that would be far more harmful.  So this is a good instance when supplementation would be of value.  Interestingly, animal liver is an under-valued source of vitamin C.  Whilst cooking liver reduces the bioavailability a little, meat-sourced vitamin C has the huge advantage it is not accompanied with sugar.  This is important as the vitamin C molecule is very similar in shape to the glucose molecule and so if you eat a lot of sugar with your vitamin C, that glucose competes with the vitamin C diminishing its absorption and utilisation.  

Vitamin C is not the only natural supplement that should be in our medicine cabinet – vitamin D taken in amounts well over and above the recommended daily intake is a great way to boost your immune system.  High dosages of magnesium can help with muscular aches and pains and reduce the incidence of muscular cramps.  Omega 3 fatty acids are part of the body’s natural mechanism to reduce inflammation and so those with high levels of systemic inflammation will benefit from a supplement high in omega 3 but crucially, also low in pro-inflammatory omega 6s.  

Having just surveyed the circumstances where supplementation might be advantageous, in what form should you take these supplements?  Yes, you could dive into those shelves at the supermarket to buy the missing nutrients in pill form, but the more robust strategy is to put foods into your diet that naturally deliver those missing nutrients.  The food form of any nutrient is always best.

Fresh, locally-sourced and (particularly for plant foods) seasonal produce will always win on nutrient content over foods mass-produced and grown out of season.  In addition I would recommend the following ‘supplements’:

1. Organ meat, particularly liver, most days.  Liver is the most nutrient dense food there is.  If you can eat this lightly cooked so that it is still very red in the middle, then you will be wanting of very few nutrients.
2. Bone broth or bone meal every day.  Bone products are rich in haem iron, vitamins A and K, essential fatty acids, selenium, zinc and manganese.
3. A fermented dairy food such as a full fat diary yoghurt or kefir.  A good source of calcium and in a form that helps boost your gut biome.
4. A good helping of oily fish every day. The best source of omega 3 fatty acids and the only source that is low in pro-inflammatory omega 6 fatty acids.
5. Fermented or sprouted vegetable foods such as sauerkraut, kimchi or sprouted sunflower seeds.  The fermenting and sprouting of these foods reduces the load of anti-nutrients contained in them.

In my next article I shall be provoking you to think again about the role of fibre in your diet.  “Not a fibre of truth” will look at the somewhat shaky science that has made us obsessed with this component of our diet.

Phil Nuttridge takes a break from his regular series of articles on specific aspects of food and nutrition, to look at the emotive issue of Obesity and its future management in the light of its correlation with poorer COVID-19 outcomes.  More information can be found on Phil’s nutrition website cuttingcarbs.co.uk or by following him on Instagram:  CuttingCarbsUK.  He also has a daily blog on coronavirus (where this article was first published) at massagehealth.co.uk/covid

I think the question of obesity will always be an emotive one. It is very easy for those who are not over weight to condemn those who are on the basis of the ‘eat less, move more’ paradigm. This is the back door to allowing the ‘gluttony and sloth’ model of obesity which is judgemental on the individual.

No-one chooses to be over-weight or have type II diabetes, but if an individual wants instead to improve their health in these two regards, they will receive conflicting advice on how to manage those conditions depending where they look. 

For fifty years we have been told to eat a low fat diet, but the gateway that creates to eating more carbohydrate is then probably the single greatest contributor to the obesity epidemic (and incidentally also the dietary pathway to metabolic syndrome). And yet, here in the UK, if they enter our health service, go to obesity or diabetes websites or open any conventional diet book, they will be told to continue with a low fat high carb diet. Short term gains become unsustainable in the longer term and the individual then struggles with their weight even more than before and feel the crushing sense of failure that creates. The judgement of the gluttony and sloth model then becomes even more unbearable.

The metabolic understanding of obesity has hugely changed in the last ten years. Obesity is now understood as a disease of hunger, it is not ‘simply’ a consequence of eating more calories than calories burned. An impaired physiological response to hunger (both from elevated insulin and leptin) is the driver of metabolic syndrome one consequence of which is obesity. Sleep, stress, nutritional profile and quality of the diet and the gut biome all contribute to the leptin/insulin axis and the neurological response to it. And yet many of the organisations trying to advise the overweight do not explain that new understanding, instead sticking to the old paradigm which has now been proven wrong. 

[The elephant in the room here is that data shows as a population we have been following calorie-controlled low fat diet for the last fifty years and yet we are the fattest we have ever been. Regrettably for those following this approach, their impaired hunger mechanisms are further damaged by calorie restriction and the yo-yo diet is created.]

Understanding that impaired hunger is triggered by the two hormones leptin and insulin then creates another problem in that our health care systems are modelled on the pharmaceutical approach to resolving ill health. So we pump our bodies with synthetic insulin to manage things and that creates more obesity. Yet, robust clinical trials over the last ten years consistently show that dietary changes can reverse the hormone imbalances far more robustly than any currently available drug intervention. This message does not get to those who need it. Even websites trying to help diabetics and the obese do not get this message consistently right.

The modern paradigm of impaired hunger and metabolic health is where the keto, low carb, real food dietary movements are coming from but yet they are still seen as the heretical fringe. There is a new breed of clinician nutritionist out there (I have trained to be one of them) and we are trying to get this message out there, but while so ever our voices are drowned-out by proponents of the old paradigm, or we are called-out just because our message is different to the old and now failed model, we cannot make progress.

That is the thing I am fighting and it is the discussion to change the prevailing message that I want to be the meaningful and enduring legacy of coronavirus. Coronavirus has found our weakness. We need to change our weaknesses not the virus.

Our metabolic health is in our control; the virus is not.

That phrase still makes my palms a little sticky.   That’s because thirty two years ago “What Change?” was the exam question for one of my finals papers (to be clear, the only question on that particular paper): Three hours to shine or three hours to dig myself down into the abyss of drivel.  

I guess I am still adding to that essay even now.  (I got a First, so my original answer must have had at least some merit).

Change is a queer beast.  I, like most, spend much of my time avoiding it.  “A creature of habit” is how most would describe me.  And yet at times in my life I have embraced big changes.  Very big changes.  Twenty years ago I gave up a career in the corporate world to become a therapist, substituting working with numbers for working with people.  I was ready for that change – suffering with ME a few years previously had made me re-evaluate my priorities.  There was no longer certainty that the world I was inhabiting was the best place for me.  

For all of us, so much of life is about change – avoiding it, minimising it, managing it, planning for it, going with it, embracing it.   “Change is the only constant in life” observed ancient Greek philosopher Heraclitus.

Coronavirus is a time of collective change – it brings change for all of us.  I was about to add ‘it is a natural disaster’ but then I hesitated – is the virus the disaster or is it more how we reacted to it that defines the disaster?  Is it how we have as individuals or societies responded to the changes triggered by the virus that will define if this is a disaster or not?

Ordinarily, change is usually a choice – most often there is the safe option of doing nothing.  If you contemplate changing your diet for example, you generally do have the option of sticking to your old way of eating (or falling back to that if the change fails). Equally if you are contemplating changing jobs, ordinarily ‘no’ is still an option.

For someone who normally avoids change, I do spend quite a bit of time thinking about it. My professional life (before Coronavirus put it on pause) was focussed on helping others with their change processes – changing posture, changing relationships with pain, changing dietary habits.  

For many, these sorts of changes have a ‘do nothing’ option lurking in the background.  This has a gravitational pull of its own and my job as a therapist is to coax patients away from that option and help keep them well away from it.  The gravitational pull of ‘do nothing’ diminishes the further you can escape it.

Change can be a very sensitive subject – that saying about leading horses to water is no less true for humans.  No one likes having change forced upon them – we all like to think we are in the driving seat.  But I often think that the measure of the (wo)man is how quickly we can take back the steering wheel when life is hijacked.

And coronavirus has certainly hijacked most of us.  

As we transition between two significant eras of human existences – ‘Before Coronavirus’ to ‘After Coronavirus’ – we are facing great changes.  And for many of us those changes are without a ‘do nothing’ option – we have already been thrust into the orbit of change far from the gravitational pull of how things used to be. 

Before I look at some of the tools of change, allow me a word or two of caution regarding the influence of others and Social Media in an era of change.

For those of us in the free-fall orbit ready for change, beware the gravitational pull created by others who are resisting change.  Coronavirus has been the great divider: There are those who have lost loved-ones to the infection; there are very many more who have not.  There are those whose jobs and careers will be little changed; there are those whose businesses and ways of working are lost forever.   For some, lockdown has created an oasis of solace, safety and comfort; others have been straining against every restriction it has created.

Each of these responses to coronavirus and lockdown make their own motivations either for change or for keeping things as they are.   No response is invalid and I believe also that no response should be used to invalidate any other.   Alas, as schools partially reopen today, a battle between these opposing responses is raging.  And as is so often the way in this modern era, Social Media is the arena where this battle is taking place.   To me this is just an example of the conflicting responses people have to change – some are comfortable with change, others are not.  Some expect the gravitational pull making change inconceivable for them, should make it equally inconceivable to you.  If you are already in the free-fall orbit of change, equally understand that there are those who do not want to be there with you.

So if you are on a trajectory of change, enforced or self-selected, beware of sabotage.  Use Social Media to promote and catalyse your changes but do not let the emotional ups and downs of that arena take you off your course.  No one is in your shoes and that cuts both ways.

I know that many subscribers to Pampering Times are self-employed hands-on therapists (like myself).  For most of us change is now inescapable.  Coronavirus has hijacked our old ways of working and we need to be back in the driving seat.   

Ever the analyst, this enforced change has made me think about my own relationship with the process of change itself.  I thought therefore that this month I would share some of those thoughts with you. 

My old life as a statistician still shapes much of how I think.  One of those ways is the way I use models as a medium for understanding and communication of ideas.  There are  various models used to describe the process of change and one I often use is known as the ’trans theoretical model’ (TTM).  In this model there are five stages of change:  

1. Precontemplation
2. Contemplation
3. Preparation
4. Action, and 
5. Maintenance

Understanding each stage of a model and the processes/thoughts required to move between the stages is often a good source of insight.  Let me start by introducing the five stages of this particular model in their clinical (non-coronavirus) context:

PRECONTEMPLATION:

This is the stage where you are unaware or in denial that change is needed. It is a comfortable place that many choose to inhabit.  Using a postural example: “Everyone tells me I have good posture” might be the view of someone in this stage and yet that same individual may have chronic lower back pain, with no history of traumatic onset and  is getting progressively worse.  Clearly a heavy dose of denial.

I only occasionally see patients at this stage in the process – if they are in denial of any problem they will not usually be out seeking a solution.  When I do see people at Precontemplation it is usually because a close relative has pushed them in my direction.  

Ordinarily, just holding-up a mirror (real or figurative) to people in this stage can be enough to help coax them out.  Promoting self-awareness is the therapist’s strongest tool here.

CONTEMPLATION

This is the first stage of acceptance that there has to be change.  That ticking off from the GP that your eating habits cannot continue unchecked or the gentle coaxing from me that uncorrected bad postural habits will continue to cause pain are all likely reasons why they have moved from Precontemplation to Contemplation.  But at this stage there is no plan, there is no commitment to act.  The language is still uncertain; there is still fence-sitting.  “I understand that losing a few pounds would help, but diets never work for me”,  is the meta-language of this stage.

This can be the most fragile stage in the process as uncertainty, lack of encouragement and fear of failure can too easily let them slip back into Precontemplation.   The barriers of denial are once more erected around the problem.

PREPARATION

“When the going gets tough the tough get going”.  And the Preparation phase is where ‘the tough’ head-to next on their journey. This is where Contemplation starts to become a plan. This is where there is the first true embracing that change has to happen. Here change is seen for the first time as the catalyst and not the enemy.  

But it is also the first place where costs and risks are weighed against the potential rewards.  “Those changes to my diet could well help me lose weight but I am not sure I have the time needed to prepare the food”.  “I can see those exercises will help with my posture, but what if I injure myself?”

Fighting ambivalence is the key to stopping someone falling back into Contemplation and never fully making it through the Preparation stage.  The stronger the ambivalence, the greater the gravitational pull back to Contemplation.  Ambivalence is expressed in the mixed feelings of “shall I, shan’t I” .  If you are coaching someone on their journey through change, you must become attuned to their use of ‘change talk’ and ‘sustain talk’:  “I really cannot carry on living in this much pain” versus “The last time I tried exercising it made it worse”.   Reinforce their talk of change; coax them away from their talk of sustaining the old way.

ACTION

This the hardest stage.  Up until now, the stages have been about mental awareness and preparedness for change.  But at the Action stage the plans of the Preparation phase are put into motion requiring physical effort and energy expenditure.  Everything feels new which can be both exhilarating and scary.  This is where the risks of change are most evident and yet because often there are long lead times between effort and reward, it is where the change journey can be self-sabotaged.  Any remaining fears and ambivalence can scupper the plan of action.  The conversation during the Action phase might sound like: “I started the new diet and at first it was really difficult to make time to make all the food from scratch. But now I am getting into a rhythm with it.” 

MAINTENANCE

Maintenance is often not considered as a separate phase but just a measure that the Action phase has been adhered to for long enough that it has become the new ‘norm’.  

“Moving with this new posture feels so comfortable now – I hardly ever have to think about it”.

There are still risks here of descending back into the old ways of thinking and acting but the longer the new actions are followed, the risk of this diminishes.

So there is the TTM model for looking at the process of change as I would have used it in the ‘pre-coronavirus’ world.

But can it tell us anything useful for the new way of things? I believe it can.  I think it is something that may allow those of us ready for change better able to embrace that change and give it some structure.  For those not yet ready for change, it may reveal where your road blocks are and help us identify those blockages in others.

There are three coronavirus-triggered change processes I want to consider in the context of this model:

1. The change many of us now face because our old way of working is no longer likely to be available to us;
2. The change process that took is into lockdown;
3. The change process we face in order to come out of lockdown.

One first thing I should note here is that all of those changes are to some greater or lesser extent externally driven.  They are going to be uncomfortable to us all until you have taken back the steering wheel. 

CHANGE 1

I do not have any statistics on this but I believe most of us would have been in the Precontemplation stage with regard our careers and working life prior to coronavirus.  All of us in denial that anything needed to change.  When you are on the treadmill of life, it is easier just to keep going.  It works.  “Don’t fix it if it ain’t broken”.

I think coronavirus and in particular lockdown, deposited many of us into the Contemplation stage whether we wanted it or not.  It held that mirror up against us to reveal some inner truths.  My own personal experience was that lockdown created some breathing space and some thinking space.  At first there was almost a bereavement stage – my working life had been taken from me and I was mourning its loss.  But then the sense of space and the freedom that that generates began to manifest itself.  

After a few weeks, I realised I had already drifted into a Preparation stage.  With hindsight there were two things I learnt during the Contemplation phase:

1. The reality of a post-lockdown world was that my old way of hands-on working was probably not going to be possible for quite some time and indeed it may never quite be the same again. I need to enter Preparation for a new way of working that would be forced on me.
2. I had enjoyed the intellectual freedoms of lockdown too much to want to let them go after lockdown!  Even if my old way of working were instantly available to me again, I might not want it!

For those of us where the old way of working is probably no longer an option, the risks and fears that might normally thwart change are no longer going to be the points of weakness in our action plans.  Specifically, one of the barriers of moving from Contemplation to Preparation in the ‘normal’ world is the excuse that “life just gets in the way”.   But of course for many of us in lockdown life is on pause:  That excuse is now laid bare! 

The Preparation and Action phases have already started for me.  New ideas, new training, new thoughts on where I will be in five years.  Lockdown is the time to be productive on plans.

What I think is interesting is my perception of others’ experience of lockdown.  Many people have not been forced into Contemplation – they are still in Precontemplation.  This could be because although they will feel the restriction of lockdown as much as the rest of us, their livelihoods will have been little changed by lockdown and will still be available to them post lockdown.  Yes, lockdown and social distancing are big imposed changes but they will be temporary – there is an ‘old life’ waiting for them to go back to.  This of course does not mean that change might not benefit people in this category (like my earlier examples of people in Precontemplation), it is just that considering change has not been forced upon them by lockdown: Lockdown has not made them stare into the mirror!

[As an interesting statistical aside, this latter group in the Precontemplation stage with little loss of income or livelihood because of lockdown are far more likely to want lockdown to continue.  They have the least to gain and fear they have the most to lose from easing lockdown.  Those like myself in the Preparation/Action stage are those most wanting lockdown to ease as we have the most to lose and the least to gain from continuing lockdown.]

CHANGE 2

Introducing lockdown was of course a change process in its own right but not one any of us had a say in.   It was sudden, not negotiated nor negotiable.  Overnight we were forced through all five stages of this model of change from Precontemplation to Maintenance.  

The moment my perception of lockdown changed was when I realised that I could put myself back in control.  Accepting that change was then so much easier once I was back at the helm:  For the first time in a long time, I actually controlled how I spent my days.  That was a truly liberating feeling.

And this is a great learning point for me  – whenever I use the change model with patients in the future,  I now know just how uncomfortable it is being dragged through the five stages of change with someone else in the driving seat.  Putting the client back at the helm is so important.  Forcing someone to the Maintenance stage is not a robust or enduring solution to change.  Note to self: In future, I need to learn to ease back more and let the clients drive their own changes!

CHANGE 3

And there is of course the third change process that we all need to face sometime and sometime soon:  Coming out of lockdown (in addition to the change process many of us are facing with regard new ways of working post lockdown).  Whether it is venturing into ‘non essential shops’ for the first time or the return of the first children to school, we cannot stay in lockdown forever.  Emerging from lockdown is just as much a five stage change process from Precontemplation to Maintenance and one we all need to Contemplate and Prepare for.

Some, like me, are itching to be out – we have been long enough in the Preparation stage and so now need to be in the Action stage.  But there are others very definitely afraid of coming out.  

This has made me aware of just how fear can be a strong motivator to stay in the Precontemplation phase.   I would say that fear has been as pandemic as the virus so far in 2020 and for many it has been paralysing.  Lockdown with its physical and mental barriers to the outside world has offered many protection, real or imaginary,  from their deepest fears.   And so it will be hard for these people to let go of their places of safety and sanctuary.  

Many of these people are still in the Precontemplation stage of their change process out of lockdown.  Even though shops and schools are re-opening and more of us can meet-up, those most afraid are still in Precontemplation.  They do not see the need to come out  yet and so are not ready to do so.  Even though the Contemplation and Preparation stages of change do not need them to have ventured out yet, those who are most afraid cannot even contemplate those stages.   Their fear has paralysed them and is imprisoning them in the Precontemplation stage.  Regrettably I think Social Media plays a disproportionate role in spreading and sustaining that fear and the most vulnerable seem to absorb that propagated fear more than most.

Here I would use some of the techniques of motivational coaching to help these people migrate to the Contemplation and Preparation stages.  Empathy goes a long way as does affirming the positives and reflecting compassion.  Avoiding falling into the ‘righting reflex’ – giving unsolicited advice – is useful too.  Understand their fear and gently place a mirror up against it for them. Let them find their own cues to releasing it.  

Help them on their journey from Precontemplation to Contemplation and then on to Preparation.  They do not have to come out yet, but get them at least thinking in that direction.

I hope those few insights may help in some way with your journey through lockdown and beyond or make you better able to understand the journey of others around you.

Coronavirus has been, and will continue to be, a date with change – let it be a fruitful union.

At a time when we cannot embrace each other, perhaps this is more than ever the time to embrace change.  

Where better to start than a view of my feet?  Well, a view of my shoes at least.

I am one of the very fortunate ones to have escaped the COVID madness of the UK and am spending 10 days in my beloved Iceland.  I was swab tested at Keflavík airport on entry and am additionally safe in the knowledge that (from a sero-prevalence taken back home) I already have the COVID antibodies.  I am therefore allowed to play in Iceland.

Remarkably, here in Iceland, life is pretty much near-normal.  Strategically positioned bottles of hand sanitiser are the only giveaway that there could be a virus lurking in our midsts.

Although the whole of Iceland is rather special – this is my 28th visit – where my feet are right now is particularly special.  The Icelandic island of Grímsey, three (typically very rough – see the photo) hours ferry journey north of the mainland, is one of those rare places left in Europe where you can retreat to be with Nature at its best and most remote.  And it is my resting place for the next few days.  

This small barely inhabited island has three claims to fame:

• it is the only part of Iceland within the Arctic Circle;
• it has its own mini “Giant’s Causeway”;
• each Summer, it is home to tens of thousands of puffins.

The last of these three is the main draw for me.  But before I tell my story of those adorable puffins and how they raise a significant point about nutrition in the 21st century, let me just throw to you one of those “Did you know….?” type trivia facts:  Did you know that the Arctic Circle moves?  Yes, each year, the exact location of the line defining the Arctic Circle shifts a little bit north or a little bit south.  

Each point on the Arctic Circle is the southern most location at which the centre of the midnight sun is still just visible at the horizon on the summer solstice.  It moves each year because there is a slight ‘wobble’ on the axis around which the Earth rotates, this wobble caused by the pull of the moon and the tides.

On the island of Grímsey, they mark the location of the Arctic circle with a concrete sphere.  The clever bit is the fact that it is a sphere – it can be rolled to the new location of the circle each year.  The photo below demonstrates this:  My truck is parked right next to a circular mark on the ground which is where the concrete sphere was two years ago. If you look carefully at the photograph you can see the sphere at its current 2020 location a little way in the distance.

Perhaps I should also mention Grímsey’s second claim to fame.  The basaltic rock structure on the south of the island is identical in geology to the much more famous, and much more visited, Giant’s Causeway in Northern Ireland.  And yet each time I have walked on that volcanic pavement on Grímsey I have had it all to myself.  Where and how better to connect with the Earth and the powerful forces of Nature that have created it? 

And connecting with Nature is my point regarding the puffins.

This is my third time to Grímsey and the puffins never disappoint.  The cosy spot where my feet are resting is on a cliff-top near the north of the island.   Today I spent a couple of hours here just ‘being’ with these rather special little animals.  There are around two dozen human inhabitants on Grímsey and as I occupied my perfect vantage point, all of these humans were about a mile south of me (the whole island is less than two miles in length).   At that precise moment there was no human in Iceland further north than me: My feet were as north as it gets! 

There is no question that puffins are adorable.  Watching them, and staying relatively still for long enough, you get a real sense of puffins at their daily business.  They are also insatiably curious.  If I make small movement they all look; they don’t fly away, they just look.  And I swear some of the bolder birds just love standing in front of the camera.  The near perfect portraiture of some of my photographs is surely evidence of that.

Not long after I took the picture of my feet, I turned and looked to the south to see that no longer was I the only human this far north.  For, sitting on the cliff just a little way behind me, was another solitary figure also quietly watching the birds.  There was however a key difference between me and this other figure:  Whereas I was clutching a camera and zoom lens, this other figure was clutching a net.

I was fascinated and so, from my perfect distance I watched.  And I have to confess that the more I watched the more I admired the skill of this man and his net.  With precise timing he would suddenly sweep the net into the air and (almost) without fail, catch a puffin within his net.  His accuracy, skill and timing were mesmerising.  

Let me cut to the chase here.  Yes, he was catching these birds so that they may be eaten.  The reactions that are almost certainly now brewing in you as you read this are really the main point of this postcard:  Our relationship with food and how it is reared and sourced.

Later that evening I chatted to the net-wielding guy and his father, as we were all staying in the only guesthouse on the island.  They talked about how their skills at catching puffins have been passed down the generations in their family.  The son had learnt from his father who in turn had learnt from his father and so on through the generations. They enthusiastically conveyed to me their knowledge and passion for these animals.  They clearly understood puffins like no one else. 

But they also talked about the recent decline in the puffin population.  How the large flocks were settling ever further north each year.  Father and son were from the Vestmannaeyjar, an island chain of the south coast of Iceland.  Up until a few years ago, they could have successfully hunted puffin at home but now, because of the puffin migration north, they too had to travel north to get good hunting.  The puffin colony on the Vestmannaeyjar is dwindling but yet on Grímsey in the far north, they now have the largest summer population of puffins ever.  For conservation reasons, whereas father and son used to be able to hunt for forty days each year, now they are restricted to just five.  And they truly understand and respect that.  Their hunting is truly sustainable.

They showed me their day’s catch.  We talked about the meat and how it is best prepared and served.  And later that evening I also ate some of their day’s catch. 

“How could you eat such a beautiful bird?” I can hear some of you ask.

Let me explain.

In the twenty first century, we have a broken food system.  To be able to offer the 99p fast-food burger or the £1.99 supermarket lasagne, we have to raise mass herds of food animals in concrete enclosures and feed them on mass-grown beans, grains and cereals.  This creates huge problems for the animals, us and the environment.  Ruminants should be raised and fed on grass  – that is what they are evolved to do.  Feeding them on beans, grains and cereals makes them obese and unhealthy (just as feeding humans on beans, grains and cereals makes us obese and unhealthy).  The nutrient profile of the meat from these poorly fed ruminants is inevitably altered and diminished.  If we rear the animals on concrete, their urine and excrement then become biohazards that need to be diluted, processed and disposed of all detrimental to the environment.  Pasture-raised animals by contrast return their wastes to the soil and the compression of their hooves enrich and sustain it making a positive contribution to the environment and the well-being of the planet.

Rather than tackling this problem at its source  – put ruminants back on grass, feed them properly and take away the 99p burger – we instead create the dysfunctional view where eating meat is seen as unhealthy and damaging to the environment.  We are shamed into eating less meat and told to turn to plant-based foods for our nutrition.  

And let’s be clear, shifting to a plant-based diet solves nothing for us or the environment.  Mass scale mono-crop agriculture is depleting soil resources necessitating less-than-environmentally-friendly GMO and agri-chemical businesses to sustain it.  Many small animals and insects are killed and their natural environments destroyed for the sake of large scale crop production.  For those humans who consume these mass-produced mono-crops, the plant material has a poor micronutrient profile compared to animal products, even from those animals raised on the wrong foods but especially compared to those fed on their ancestral diet.  Many of the micro-nutrients, found in plant food are in the wrong biochemical form to be readily utilised by humans.   We also now know that many plant foods contain chemical defence weaponry (plants don’t naturally like to be eaten!) that disrupt our own metabolism and those of the bacteria in our guts when we eat them.  Farting and bloating are after all the hallmarks of plant based foods!

So how do we change things to get it right?  We need to eat food that has been grown and raised in the most natural way possible. 

And this is where the puffin comes in.  Thinking of it as a food source, and the puffin has indeed been a natural food source for island communities in the northern part of Europe for centuries, you cannot get more ‘free-range’ or ‘organic’ than that.  It is an animal that has eaten what its natural diet dictates and has lived how its genes determine.  There is nothing artificial within its flesh.  It is not a polluter of the environment.  Consequently, the puffin breast I ate that night was probably the most nutritious food I had eaten for a while.  It also probably had the smallest carbon footprint – the restaurant where I ate it was only a short walk from where it was caught.

And so this demonstrates one of the modern myths of meat eating.  It is not meat eating per se that is harming us and damaging the planet, it is how we are raising and rearing our meat.  And in fairness, it is far from the majority of our meat.  It is only the meat that is in the 99p burger and the £1.99 lasagne that is typically at fault.  If we did not drive the demand for these products we would not create the market for poor quality meat.  Don’t demonise all meat because a small sector of the meat economy is broken and dysfunctional.  

OK so we can’t all eat puffin and nor should we.  Here in the UK we can though access some similar ‘natural’ meats:  Wild venison, rabbit and pheasant hunted in season are tapping into animals that have eaten and lived as their ancestry determines.  Lamb is pretty close too – it is hard to feed sheep on anything other than grass and pretty much all our British lamb is allowed to roam free on natural grassland.  Fortunately in the UK too the vast majority of our beef cattle are raised in pasture (and pasture land that is mostly not suitable for crop agriculture despite the protestations of some vocal plant-based advocates).  But beware the cheap imports – if there is beef in your 99p burger it has almost certainly come from somewhere where shortcuts have been taken in the animal welfare and its diet.   You are what eat has eaten!

Be a canny meat shopper, but still be a meat shopper.  Meat is the most nutrient dense food on the planet – source it well and it will feed you well.

Loving meat is a good and easy thing in Iceland as Icelanders also love their meat.  Their lamb and beef are some of the sweetest you will ever taste due to the rich volcanic mineral content of the grass they eat from the spectacular scenery in which they graze.  Icelandic duck, goose and reindeer are also ancestral delicacies not to be missed – all of it about as organic and free-range as it gets.  I am rather partial to their fermented shark too, but that is another story!

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!

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 the how we have been misled by nutritional studies over the last fifty years.  Headlines that start “Diet study shows…..” are all too often leading us into a trap and Phil shows you how to avoid such traps.  More information can be found on Phil’s website cuttingcarbs.co.uk or by following him on Instagram:  CuttingCarbsUK

I have a theory about swearing. 

I have five good friends who come to me for manual therapy treatment and if I press hard enough on their tight muscles during those sessions they swear.  I have six other good friends who tell me that they do not have tight muscles and no matter how hard I press, they do not swear.

My conclusion is therefore that having tight muscles causes you to swear.  And of course, you can see I have the data to prove it.  Hence forward, let this be known as ‘The Nuttridge Law of Swearing’.

Now of course (I hope) you see that this is utter nonsense.  Just to be clear, the nonsense is as follows:

1. I have ignored the fact the there are people who have tight muscles who do not swear and there are people who swear who do not have tight muscles.  For the Nuttridge Law to work I have to ignore these.
2. My data is only for eleven of my friends. The other seven billion people on the planet may not behave in the same way.
3. I have not defined what I mean by swearing. Does a ‘strewth’ count as swearing or does it have to be the sort of language who might hear on Game of Thrones? My friends are definitely more at the ‘strewth’ end of the spectrum and yet I am implying that the Nuttridge Law applies to the whole spectrum.
4. I have completely ignored that it is my pressing on the tight muscles that elicits the swearing, yet the Nuttridge Law implies that it is enough for there to be tight muscles for the swearing to ensue.
5. I make no mention of how often I prodded the people and or how hard I prodded the people or how long I spent trying to find spots that would elicit swearing.  Surely that must make a difference?
6. The five friends who I identify having tight muscles are so determined from my prodding; the six friends who do not are ‘self-reporting’ their lack of tight muscles.  Maybe the friends with knots warned these other friends that if they confess to having tight muscles, it’s going to hurt!  
7. No matter how strong the apparent link between swearing and tight muscles in my data, the Nuttridge Swearing data assumes causation(tight muscles cause swearing).  The data however no more strongly suggests that tight muscles cause swearing than it suggests swearing causes tight muscles.
8. I have completely ignored the possibility that things other than tight muscles might better correlate with swearing but yet these other things might also be correlated to tight muscles. For example, having a stupid boss at work might both give you tight muscles and increase the likelihood that you swear.  

You can tell I am a statistician – I have managed to create eight bullet points of analysis from just two sentences of data.  As one of my colleagues from the days when I had a proper job once said, Phil sure knows how to put the ‘anal’ into ‘analysis’!

But there is a very serious point here.  All of these elements of nonsense have been used to fool you – yes, I mean you – and me and everyone else into believing all sorts of stuff about food and nutrition.  What I am referring to here are those newspaper headlines “Study shows that eating <food x> causes <illness y>”.  Or “Study shows that <diet x> is good for you/bad for you (delete as applicable)”.

In the context of my tight muscle/swearing data, it is pretty obvious that the wool is being pulled over your eyes.  But amidst the complex data of the reported nutrition studies, it is far less obvious. And let’s face it, unless you are a geek like me you are not going to delve below the headline allowing you to be drawn in the direction the headline wants to take you regardless of how flawed the study is.  No wonder we are all confused about what to eat and what not to eat.

What I would like to do in this article is give you two real examples of how we we have been led down the garden path with nutritional studies.  We all want to believe that science is robust and to be trusted; what I want to show you is that you have to be rather more discerning.

FAT CAUSES HEART DISEASE, RIGHT?

In my earlier article about Fatphobia, I described the ‘Seven Countries’ dietary study. To recap, this was an analysis of the eating habits of seven countries and how that correlated to heart disease rates in those countries.  The data seems to demonstrate perfectly that countries with low consumption of fat had the lowest rates of heart disease; those with the highest consumption of fat had the highest rates.  So convincing was this data, that this study has become one of the most cited scientific studies of all time.  Without question it is the bedrock on which the ‘fat is bad’ paradigm has been built.

But just how robust a study is it?  Specifically, does it fall into any of the nonsense traps of the Nuttridge Law of Swearing?

Yes it does.  Spectacularly.

In fact, this pivotal study that has shaped most of our nutritional thinking for the last fifty years fails on pretty much all of the items listed in my demolition of the Nuttridge Law:

1. The author of the study chose to look at data from just seven countries but he actually had data from twenty-two countries. He chose to ignore countries with high fat consumption and low rates of heart disease and also countries with low fat consumption and high levels of heart disease – these countries would be ‘inconvenient’ to his conclusions.  It is the same as me ignoring people who have tight muscles but do not swear and people who do swear but do not have tight muscles. 
2. The study only looked at the detailed food diaries of a relatively small number of people in each country and then, only on a very small number of occasions.  It is like saying that my eleven friends’ swearing habits are a true measure of all seven billion people on the planet.  Even if he had used the data from all twenty-two counties he had at his disposal it would only have been a fraction of the world’s population and only sampled on a small number of occasions.  Astonishingly he only collected data from men; not one woman’s dietary habits was measured in the study.  Not one.  Intentionally only measuring the correlation between fat and heart disease in men but then applying the results to women too is an ‘interesting’ statistical approach to say the very least.
3. There were some breathtaking holes in his data collection.  He chose, for example, to ask a Greek orthodox community about their fat consumption during Lent.  Is it any surprise then that their reported fat consumption was low?  Was it how I pressed the muscles and when I pressed them that caused the swearing in my data?  Similarly, was it the way the Seven Countries’ data was collected that showed low fat consumption? 
4. Interpretation of this study has fallen hook, line and sinker into the causation trap.  The data, even if it had not fallen foul of the points above, would only show correlation not causation.  In fact if you recast the data from the original study there is a stronger correlation between sugar consumption and heart disease (expected) and even between TV ownership and heart disease (not so expected).  Yet the study is used to show high fat diets causeheart disease. It is just like my swearing data being used to show tight muscles cause swearing.  And the sugar correlation is like my analogy of the stupid boss who might be correlated better with both tight muscles and swearing.  Because the author of the study was so convinced that fat was the villain he ignored the better correlation with sugar.

I cannot emphasise just how pivotal this Seven Countries study has been in implanting the paradigm that eating fat causes heart disease.  And yet it fails on so many of the flaws of the Nuttridge Swearing data.  The next time you refrain from having that piece of cheese, or get tempted by that ‘low-fat’ yoghurt, or say ‘no’ to that drop of cream on your bowl of strawberries or baulk at that three egg omelette, just remember that the ‘fat is bad’ reflex engrained into us all is based on a study scarcely more robust than my swearing and tight muscle data.

BACON CAUSES CANCER, RIGHT?

In 2015 there was a news headline ‘Eating bacon increases your risk of cancer by 20 per cent’.  Horror, horror, horror.  In the interests of keeping the bacon butty, let us examine how this study measures up against the Nuttridge Swearing data.  Can I save your bacon?

Let me sort-out the numbers first, after all, that is what statisticians do.  A twenty percent increase in cancer risk sounds truly horrific, doesn’t it?  But there is some naughtiness here – there is one very vital word missing from that headline. 

Going beyond the headline, the numbers in this study are: For every hundred people in the ‘no/low bacon’ group, five got cancer;  for every hundred in the ‘high bacon’ eating group, six got cancer.  So, where did the 20 percent in the headline come from?  Well an increase from 5 per 100 to 6 per 100 is a relative increase of 20 per cent.  But the absoluterisk of getting cancer only went up by one per cent.  And when it comes to cancer, it is absolute risk that matters.

Of course a newspaper headline ‘Eating bacon increases your risk of cancer by 1 per cent’ isn’t so catchy is it?  If you were told that eating four or more rashers of bacon every day for the rest of your life would only increase your risk of cancer by one percent, would you be worried?  For comparison, regularly drinking moderate amounts of alcohol increases your risk by far more than that.  So, by omitting the word ‘relative’ from the headline and working on the assumption that very few people would delve into the data, the headline writers let you believe eating bacon is far worse than the data actually suggest.  But why would they do that? 

Money.

It was the shady informant character called ‘Deep Throat’ who told the journalists investigating the Watergate scandal that they should “follow the money”.  And so it is here too: This bacon study was sponsored by a breakfast cereal manufacturer.  Yes, the people who do not want you eating bacon but instead want you to consume their high profit margin, high carb and high sugar breakfast mueslis and cornflakes were behind the shenanigans here.  So (and thankfully I can say that the Nuttridge Swearing data does not fall foul to this one) always, always beware of who sponsors a food study.  

Let me ponder the numbers a little bit more in this study.  Remember my stupid boss analogy in the swearing data?  How can we be sure that there is not some other unreported factor at play here that has a stronger link with cancer?

Well, if you again delve into the data of this bacon study, you will see something rather odd.  The people who ate the most bacon also drank the most alcohol, smoked the most and exercised the least.  By a significant margin on all counts.  So, if the bacon eating group have a higher rate of cancer, is it because of the bacon or is it more likely the booze, fags and sloth? The cereal manufacturer does not want us to think in those terms so these ‘facts’ were excluded from the headline. In fact, alcohol and tobacco have such a strong correlation with cancer risk that for those in the bacon-eating group to have ‘only’ increased their risk by 1 per 100 (tobacco alone would increase the risk by around 4 per 100), maybe eating bacon was in some way protective for the smokers and mitigated most of the cancer risk from smoking. Now there’s a good reason to tuck into some bacon!

Of course, even if we ignore the skulduggery over the numbers, as with pretty much all such food studies, the bacon study wants you to confuse correlation with causation.  Just as I wanted you to believe tight muscles cause swearing even though my data only showed correlation,  so it is with bacon consumption and cancer.  And with only a one percent difference in cancer rates even though they smoked and drink the most, bacon-eating only had a very weak correlation to cancer at best, and maybe even a beneficial link.

There is one further point which also applies to pretty much every food study that I want to conclude with.  

Recall how in my swearing data, it was bit unclear whether it was the presence of tight muscles or me pressing them that related to swearing?  And remember how those without muscle knots were self-reporting? You could say that my data collection methods were a ‘bit vague’.  

In the bacon study, participants were given a questionnaire asking them to list what they had eaten and drunk in the previous week and what activity they had undertaken.  If I gave you a questionnaire and asked you the detail of what you ate last week, how accurate do you think your memory would be?  How much could I trust you not to over-report the foods that you think are ‘good’ for you and under-report the foods that are ‘bad’ for you?  How could I be sure that you don’t forget those biscuits you had last Thursday or that lump of cheese you had just before bed on Saturday?  Or that sneaky top-up of wine on Sunday?  

And yet, because it would be unethical to keep people isolated in a laboratory and control every aspect of what they eat and do, pretty much every nutrition study has to rely on self-reporting questionnaire data like this. Shockingly, even though this bacon study followed the cancer outcomes of the participants for ten years, they were only once asked to record what they ate.  How robustly can I assume that what you ate last week (or rather, what you saidyou ate last week) will be representative of what you will actually be eating in ten years’ time?

Is it any wonder then that the results of nutrition studies can seem contradictory – today’s superfood is tomorrow’s cancer-causing horror?

So, perhaps eating saturated fat is not linked to heart disease and perhaps eating bacon is not linked to cancer.  Of course those companies that want you to eat their processed carbs instead of natural fats and those that want you to eat their ‘healthy’ breakfast cereals instead of bacon will wave these studies at you.  And if you are too trusting of science, you will believe those studies.

Let me give you a simple tool to help de-clutter some of this nonsense.  Let’s have a close shave with something called Occam’s Razor.

Occam’s Razor is a philosophy that is really an appeal to that rare commodity – common sense.  The Razor essentially suggests that when you have competing hypotheses, the one that requires the fewest assumptions is usually the best one.  In other words, the simpler the better.

Let’s apply Occam’s Razor to the hypothesis: “Eating saturated fat causes heart disease, eating unsaturated fats and carbs reduces the risk of heart disease”. 

One hundred years ago, there was very little heart disease. Then, we ate more saturated fat than we do now and far fewer refined and processed unsaturated fats and carbs.  Today we have higher levels of heart disease.  We now eat less saturated fat (because we have been told to), we eat more chemically created unsaturated fats (because we have been told to) and far more processed and refined carbs (if we have less fat on our plate, we need to fill it with something else).

Can it really be the case that we now eat less of something that according to our hypothesis causes heart disease (ie saturated fat) and more of the foods that are meant to be protective (unsaturated fats and carbs) and yet we now have much higher levels of heart disease?  Compared to a hundred years ago, we now eat less of the (alleged) bad foods and more of the (alleged) good foods and yet we get more heart attacks. It just does not make sense.

Wouldn’t it be far simpler (Occam’s Razor) to assume that the thing we eat less of (saturated fat) in an age of more heart disease is actually the thing that protects against heart attacks?  Eat less of it, less protection.  And the things we eat more of (unsaturated fats and carbs) in an era of more heart attacks are the more likely cause of those heart attacks?  Eat more of them, more heart attacks.

Simple.

So beware. If you see a headline “Study shows……” be very suspicious.  Do not let a journalist’s spin on a study, probably sponsored by a food company and with probably some very dubious data collection techniques that almost certainly can only at best show correlation rather than causation, sway you into thinking that a food or diet is good or bad for you.   Healthy cynicism with a good deal of common sense is the best diet. 

In my next article I shall tackle the tricky subject of food supplements.  “To supplement or not to supplement, that is the question” looks at the case for pills over food.

To read the previous article click here

Phil Nuttridge continues his series of articles looking at the modern take on diet and nutrition.  He explodes many of the dietary myths that have 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 explores the ‘cholesterol is bad’ myth and aims to make you love this clever little molecule rather than fear it.  More information can be found on Phil’s website cuttingcarbs.co.uk or by following him on Instagram:  CuttingCarbsUK

Marti the Martian loved his job.

Marti had worked in the department observing alien worlds for quite some time now and just six months ago he had been promoted to the section watching Earthlings.  This was a particularly rewarding job as humans proved to be the most intriguing of all aliens.  His most recent project had been to try and understand why so many Earthlings would choose a man called Trump to be their leader.  That project had been a been a bit disappointing as, try as they might, no conclusive answers were found.

Marti was therefore pleased to be assigned to a new project.  This time he was to look at why there are so many accidents on Britain’s main road network.  Armed with his notebook and pen (he was very old-school), Marti hovered in his flying saucer observing the motorways and trunk roads in the UK.  He saw the aftermath of many road traffic accidents on the network, sometimes involving just a few cars, sometimes involving many.  Sometimes lorries were involved, sometimes buses.  Sometimes the accidents just caused a minor disturbance in traffic flow; sometimes the roads became blocked. 

Then he started to notice a pattern, something Marti was very good at.  He noticed that in the aftermath to pretty much every accident there were ambulances.  If the accident was small there might just be one ambulance.  If the accident was rather larger there would be more.  Sometimes there would be so many ambulances that they would block the road completely causing snakes of traffic to back-up behind them, leading to road chaos.  And it was a perfect correlation: Where there was a stationary ambulance on the roads, there was an accident; when there were no ambulances, or the ambulances were moving freely, there was rarely a traffic accident.  

The more he observed, the more it confirmed this correlation.  Ambulances were bad news as far as traffic accidents were concerned.  He even refined his theory after a bit more observation by making a distinction between two sorts of ambulances: There were the “bad” ambulances, the ones that had blue flashing lights and then there were the “good” ambulances that did not.

Excited with his conclusions, Marti zoomed back home in his flying saucer and compiled his report.  Ever keen to impress his bosses he even made a Martianitarian suggestion of how his race could help the poor Earthlings:  let’s invent a ray-gun that selectively destroys “bad” ambulances and point it at the Earth.  In that way, so many road traffic accidents would be prevented that the Earthlings would be ever grateful to Martians, or so Marti believed.

So, the story of Marti and his ‘ambulance theory’ is of course analogous with a very serious message.   Let me translate the story:

• For the main roads and motorways in the story, read our blood arteries
• For the road traffic accidents, read damage to artery walls.  Therefore, a clogged road in Marti’s story =  a clogged artery, and traffic chaos = a cardiovascular event such as a heart attack or angina attack.
• For ambulance, read cholesterol and therefore, for “bad” ambulance, read “bad” cholesterol and for “good” ambulance, read “good” cholesterol.
• And finally, for Marti’s selective ray-gun, read statins.

Now re-read the story with these translations.  

Whilst this analogy is light-hearted, the story of cholesterol is not.  If you are of my age (mid fifties) you will have grown-up with the perpetual fear of dietary cholesterol.  Eggs are the enemy or so we have been told.  Eating cholesterol raises your blood cholesterol.  Blood cholesterol clogs your arteries and clogged arteries will give you a heart attack.  And then, like parents instilling fear in children with tales of the bogeyman, by sleight of hand, saturated fat gets thrown into the horror mix as well.  Eat saturated fat and that clogs your arteries too, though no one really explains quite how that fits with cholesterol.  Then it gets fudged even more, do we mean saturated fats or all fats?  Synthetic fats, created by big business and for big profit, seem exempt from this “fat is bad” story.  I grew-up being told that polyunsaturated fats in margarines were better for us than natural saturated fats.  No one told me how the synthetic forms of polyunsaturated fats are strongly linked to cancer and heart disease.  But did you also know that lard (how my generation have been told to boo-hiss this fatty poison) is actually only 40% saturated fats; 60% of lard is naturally occurring mono- and poly-unsaturated fats?  If unsaturated fats in margarine are healthful, why are they not also healthful in lard, the ones in lard having the advantage of being natural and not manmade?

There is an elephant in the room of course.  Hominids, of which Homo sapiens is just one species, have been eating fat in all its natural forms for millions of years.  For certain populations and at certain times of year, fat has been almost the entirety of our diets.  And yet heart disease is a new phenomenon and has only been a clinically identified condition for less than a hundred years.  Can eating something we have been eating for millions of years, suddenly (in evolutionary timescales, the last one hundred years is just the blink of an eye) be causing heart attacks?  In that same one hundred years we have been eating way more sugar, way more grains, way more refined carbohydrates and way way more of the artificial fats. And yet we exonerate all of those additions to our diet as the cause of heart disease and instead blame naturally occurring intrinsic fats and cholesterol which we have always eaten.

Let me begin the rehabilitation of cholesterol.  If you really believe that cholesterol is bad for us, you are in for quite a shock when you see this list of cholesterol’s virtues:

1. Cholesterol is essential for the building and maintenance of the walls of all cells in our body.  Every cell membrane is made from a mixture of cholesterol, fat and protein and its integrity and function is essential for controlling what enters and leaves the cell and so, for all aspects of cellular communication.  Without cholesterol you will die.
2. Cholesterol is an essential precursor for all steroid hormones in the body.  Cholesterol is therefore vital for the hormones that control (for example) blood sugar levels, the stress response, mineral balance, blood pressure and the reproductive system.  Without cholesterol you will die.
3. Cholesterol assists the body with fat digestion.  Bile salts are synthesised from cholesterol and are essential for the digestion and therefore absorption of fats and the fat soluble vitamins (A, D, E and K).  Rather cleverly, Nature knows this and virtually every natural source of fat includes cholesterol to aid its digestion. Without cholesterol you will die.
4. Cholesterol is a key component of the fatty myelin sheath on nerve cells, required of their efficient function.  A quarter of your body’s cholesterol is unsurprisingly therefore found in your brain.  Cholesterol is consequently essential for movement, sensation, thinking, learning and memory.  Without cholesterol you will die.
5. Cholesterol is essential for the production of Vitamin D in the body.  Sunlight hitting cholesterol in the skin cell membranes, turns the cholesterol into Vitamin D.  This vitamin is proving to be one of the most important of all Vitamins, so much so that in some clinical circles it is now considered more of a hormone than a vitamin.  Vitamin D controls immunity, calcium and phosphorous metabolism, bone health and mental health.  Without cholesterol you will die.

Without cholesterol you will die.  

Our evolved bodies know all this, and probably more that we do not yet know.  We have a very sophisticated metabolism that controls the level of cholesterol in our blood.  If you eat less, you liver produces more; if you eat more your liver produces less just to keep your serum levels of cholesterol at optimal levels.  So cutting eggs (and other sources of cholesterol) out of your diet will not impact your serum levels of cholesterol as the liver will manage the situation.  Statin medications interrupt the enzymes in the liver that perform this control and so have to be bad news.  Though I would caution that those very few of the population with congenital hypercholesterolemia who have an impaired cholesterol regulation mechanism may have to resort to medication to manage this genetic problem.  But this condition is very rare.

The next myth about cholesterol is that there are not “good” and “bad” forms. There is only one form of cholesterol and as I have shown above it is always good.  There are however multiple forms in which cholesterol is transported around the body.  The ‘taxis’ cholesterol uses are know as lipoproteins and they come in quite a number of forms.  The two you may have heard of are LDL and HDL – low density lipoproteins and high density lipoproteins.   It is a commonly held belief that HDLs are the “good” cholesterol and LDLs are the “bad”.  Yes, a high concentration of HDLs in your blood IS correlated with good health outcomes.  The evidence that high levels of LDL are bad for you is very circumspect.  To use the statistical jargon, the correlation between raised serum levels of LDL and cardiovascular outcomes is very low and contradictory from different studies; there are other blood measures that have stronger correlations with heart disease and I will come to those later.  We do not hear a great deal about the virtues of raising the levels of HDL to improve health outcomes because there is not a drug to do that job for us.  Diet is the best way.  Eat lots of natural intrinsic fats and cut the carbohydrates in your diet and your HDLs will stay protectively high.

In addition to HDLs and LDLs, there are more forms of cholesterol ‘taxi’ that we hear less about.  I would cynically argue the main reason we hear less of these variants is that Big Pharma does not have medication-based ways of controlling the levels of these other forms of lipoprotein.  The one I shall major on here is VLDL – very low density lipoproteins.

If you have been able to persuade your GP to carry out a full lipid panel (not just the standard single measure cholesterol test which is in itself meaningless) then you will have had this measured.  It is usually referenced as ‘Triglycerides’ and this one IS correlated with heart disease outcomes.  But here’s the thing:  Do you know where triglycerides come from?  Excess carbohydrates.  Once your have replaced all your glycogen stores (the form of carbohydrate we store in the liver and muscles) from digested carbohydrates, then the liver will convert any excess sugars to triglycerides and put them in VLDLs to transport around the body ready for fat storage.  Yes, the dietary villain I keep telling you about is the root cause of the ‘cholesterol’ measure that is correlated with cardiovascular illness: Carbohydrates.

Let me quickly review some of the prominent evidence that the ‘cholesterol is bad’ story is wrong.

1. Women.  Yes, half the population of humans bely the idea that total cholesterol is bad for you.  Females have on average higher levels of total serum cholesterol than males and yet have significantly lower incidence of cardiovascular disease.  This fundamentally contradicts the hypothesis that higher cholesterol equals higher risk of heart attacks.
2. The Framingham study, started in 1948 is the longest ongoing study of health outcomes.  Based in the town in Massachusetts, the study is following the lives of over 5,000 participants and their subsequent generations (the study is now on the fourth generation inhabitants) looking at health outcomes against lifestyle factors.  This study shows that people who eat the most cholesterol and eat the most saturated fat, weigh the least and have the best cardiovascular outcomes.  Furthermore, the observational data shows that lowering of blood cholesterol levels over the age of 50, is correlated with WORSENED health outcomes.
3. The Women’s Health Initiative Dietary Modification Trial (WHIDMT).  Whereas Framingham is the longest duration observation study, the WHIDMT is the most ambitious intervention study to date.  This study took 49,000 post menopausal women and divided them into two groups:  One group was given advice, coaching and encouragement to follow a low fat diet; the other control group received no support or coaching in dietary change.  The women were then followed over a seven year period and their health outcomes examined.  The women in the intervention group (low fat diet) had no measurable improvement in health outcomes than the control group despite eating significantly less fat.  In fact, those women in the low fat diet group who had heart disease at the start of the trial, had WORSENED health outcomes by the end compared to similar women in the control group.  Furthermore, the study showed that those who had type II diabetes at the start of the trial were 39 percent more likely to develop heart disease even when treated with statins.
4. The Los Angeles Cardiac Admission study looked at the blood lipid results of 136,000 patients admitted to hospital with a coronary heart event.  This data showed that those admitted with heart attacks had lower than population average levels of total blood cholesterol and lower than population averages of LDL carriers.  If the ‘cholesterol is bad’ hypothesis were true, then you would expect patients admitted with heart events to have the highest blood cholesterol and LDL levels but this study conclusively showed they had the lowest.
5. A meta study collating data from 19 individual studies of patients over 60 years old, showed that of the combined 68,000 patients in these studies, those with high levels of LDL lived as long and in many of the studies longer, than those patients with lower levels of LDL.

Unlike the studies you hear about claiming cholesterol is bad and statins are good, all of the above studies are large scale studies and mostly studies observing patients over long periods of time.  Unlike the majority of studies supporting the ‘cholesterol is bad’ hypothesis, these studies are not funded by pharmaceutical companies. 

So, if cholesterol is not the villain in heart disease, how did it get the bad rap?  The ‘cholesterol is bad’ story started in the middle of twentieth century when there was an urgency to find a cause and hence solution, to the then rising tide of cardiovascular disease.  The early studies of arterial plaques showed that cholesterol was indeed present in these accumulations on the walls of arteries.  And because the clogged artery theory of cardiac disease assumes that it is the detaching of these plaques from the artery walls that causes the heart attacks, the eagerness to solve heart disease meant that cholesterol got the blame.  Because the studies showed that cholesterol was in the plaques they concluded that cholesterol causes heart attacks; they confused correlation with causation. Remember Marti and his ambulances – they were present in the road traffic accidents but that does not mean ambulances caused the accidents.  In the same way, just because cholesterol was at the crime scene did not mean it was guilty.  But, with the creation of statin drugs that are able to lower cholesterol levels it was game, set and match against cholesterol.  The ‘cholesterol is bad’ paradigm was born in the climate of eagerness for a solution.  Mortality from cardiovascular disease has indeed reduced since this time but most (if not all) of this decline has been due to the reduced levels of smoking in the population and better and earlier detection techniques rather than dietary or pharmaceutical intervention.

Now statins are an industry in their own right and estimated to be worth an excess of $35 billion a year to pharmaceutical companies.  A lot of financial interest is therefore vested with propagating the cholesterol paradigm, despite significant and robust evidence from studies casting significant doubt on the original ‘cholesterol is bad’ hypothesis.  

A bit conspiratorial?  Well yes, but do consider that the health profession once deemed smoking safe:  A survey in 1961 (only a little before my time) showed that sixty per cent of GPs thought smoking was safe and 41 per cent of GPs actually smoked.  There were studies, funded by tobacco companies, that showed smoking was safe and even conferred health benefits. With fifty years of hindsight we know this is ludicrous; maybe someone writing about the history of statins in 2070 might conclude the same.

Let me conclude with another piece of the cholesterol jigsaw.  Remember how it was found that cholesterol was always present in arterial plaques, but that this correlation got confused with being the cause of heart attacks?  One of the more recently understood functions of cholesterol that I did not list earlier is repair of damage to arterial walls.  Yes, it is truly like one of Marti’s ambulances!  So if we want to reduce the incidence of heart disease we need to reduce the number of instances of damage to artery walls and NOT reduce the number of cholesterol molecules that are needed to repair them once damage has occurred.  Just like we do not want to reduce the number of ambulances on our roads, we instead need to reduce the number of road traffic accidents.  Ambulances are needed just as cholesterol is needed.

And the root cause of damage to artery walls?  Inflammation.  And the cause of systemic inflammation?  Whilst there are many causes, chief amongst them are excess levels of insulin associated with insulin resistance.  You may remember I described this condition in my earlier article entitled ‘A sweet carb named desire’ and how this was linked to obesity, type II diabetes and many other conditions.  Well we can now put cardiovascular disease on this list and yes, eating too much sugar, one of the long-term triggers for insulin resistance, is the key dietary villain.  

So if you are taking medication for any of the chronic non-communicable diseases of the twenty first century, chances are all you are doing is taking medication to overcome the effects of excess sugar and refined carbohydrate in your diet.  Mary Poppins in her song got it nearly right but just the wrong way round.  She should have been singing ‘a spoonful of medicine helps the sugar go down’.

In my next article I will look at the scary world of dietary studies.  Open any newspaper and there will be a headline starting:  “Study shows……..” and then some food substance we had previously been told is good for us is now bad for us or another that was bad for us is now good for us.  And then next week it is all switched around.  In “10 out of 8 Cats Probably Don’t Care”  I will look at how all is not as it seems in dietary research.

To read the previous article click here

Phil Nuttridge continues his series of articles looking at the modern take on diet and nutrition.  He explodes many of the dietary myths that have 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 some simple rules on how to fill your plate for a healthier outcome.  More information can be found on Phil’s website cuttingcarbs.co.uk or by following him on Instagram:  CuttingCarbsUK

Open any fitness or health magazine and there will be some new magical diet plan to help you lose weight and get healthier.  Cut the carbs, cut the fat, cut the meat; count your calories, count your points, count your syns; skip a meal, skip a day.  They are all out there craving your attention.

They all have differing levels of science behind them.  They all claim to have had their successes.  But there is one variable that none of them can take into account: You.

You are an individual.  Your genes, your gut bacteria, your preferences, your likes, your dislikes, your knowledge, your experiences are unique.  No one else has your particular combination of all of these factors and yet all of these things influence your relationship with food.  

It is therefore without question unreasonable to expect one particular dietary strategy to work for each and every one of us.  One size does not fit all when it comes to diets.  Inevitably some strategies are going to work better for you than they are going to work for me.  The perfect solution for me may prove not so ideal for you.  So how can anyone ever take a diet plan seriously?

Well the first thing I would say is that, and maybe this is being cynical, some diet plans with little science or evidence of efficacy behind them will exploit this uncertainty.  If no diet can ever be guaranteed to help everyone, surely it cannot do any harm to try the latest fad?  Of course that is what the creators of the latest fad diet want you to believe.  And once they have your money, do they really care?

I care.

Whilst my series of articles on nutrition have some distance yet to cover, I think it is quite timely at this stage in the series to start distilling some points of general ‘wisdom’ with regard changing food and eating habits.   When you see this list, some I hope are common sense. I have chosen just six of my ideas here, but hopefully they are worthy discussion points and quite literally, good food for thought.

1. Avoid the Diet Transplant

We have all been there.  We open the latest issue of a ‘health’ magazine or the weekend supplement of the newspaper and there is the perfect meal plan.  Every breakfast, lunch and dinner is mapped out for us for the next month. Follow the plan and all our troubles will be over, they claim.

Alas it is not that simple.  As I mentioned earlier, what we eat and the way we eat is determined by many factors. Your genes, your food likes and dislikes; what you have time to prepare; what is available in your local shop; what your mother made for you when you were a child; what others in your household like to eat; what hours you work; when you workout; when you sleep and the list goes on. All of these things shape your daily eating habits.   And so your ‘diet’ – the term for what and how you eat – is an evolved concept based on how all of these factors have shaped your eating habits over your entire life.

Similarly, the author of the meal plan you have seen in that magazine will have factors shaping the way he or she eats and those will be reflected in their meal plan. But the key thing is that the factors influencing the author’s way of eating are almost certainly very different from your own.  They may love avocados, you may hate them.  They may have lots of time in the kitchen to bake their own bread, you may not.  They might have enough money to have everything hand-squished, you may not.  They may live alone, you might have three ravenous teenage boys to feed.

But you are still enticed with the promises of that perfect meal plan and so you give it a go.  I call this process the ‘diet transplant’:  Under the anaesthesia of the promised health benefits, you undergo the surgical procedure of extracting the diet you have spent a lifetime evolving and transplant it with the diet from the magazine.  And at first you will cope.  Whilst you are in the expectant honeymoon stage of the transplanted diet you will do anything, no matter how bizarre the ingredient, how fiddly the preparation, you will do it in the expectation of those promised shed pounds. All the while though, the influences that have spent a lifetime shaping the way you eat, are still chipping away at you.  You hate avocados but you will give them a go because that is what the meal plan says. You might now be spending twice as long in the kitchen as before, but you will do it clutching to those images of slim healthy people you saw in the magazine alongside the meal plan.  Your body is trying to reject the transplant, but your willpower overcomes the attempts to reject it.

As time progresses though, your willpower is put more and more to the test.  All those influences that have shaped your preferred diet over all those years, now push ever harder against this diet transplant.  

And then it comes:  That day from Hell.  What little resource of willpower you had left is now exhausted because of the way your boss shouted at you, or how that credit card bill somehow gained a few extra zeros, or because your husband threatens to divorce you if he sees one more avocado.  And so it crumbles, the transplanted diet is completely rejected and you run straight back to your old diet for comfort but now with an added sense of failure to boot.

We have all been there.

My pragmatic solution for this is to use the staircase approach to dietary change. Set a specific goal – let’s say, to cut your bread consumption by three quarters –  then divide the journey between where you are now and where you want to be into manageable steps.  The first step could be ‘make every sandwich an open sandwich’.  The next step would be to ‘replace sandwiches twice a week with a salad’.  The third step might be to ‘buy or make some low carb bread for sandwiches’.  Try the first step; once that is working well for you, take the next and so on.  If a step becomes too much, you only fall back one step from which you can try again. 

You might have several staircases on the go at once.  You might have the bread staircase running in parallel to a staircase which is cutting your synthetic fats by half or a staircase cutting potatoes and pasta from your diet.  Each staircase is progressing one step at a time, but each is on its way upwards.

Avoid the diet transplant, instead take the staircase to success!

2. If your great great grandmother wouldn’t recognise it as food, don’t buy it

In much of the current writing on food and nutrition there is one concept that really cries out to me:  The twenty first century will be remembered as the rise of the food-like substance and the decline of real food.  Since when has mushed, mashed, minced, chemically prodded and poked soya mince been a real food?  What part of a chicken is a ‘nugget’?  How did we end-up thinking a nutritious breakfast could be found in the form of a ‘biscuit’ with 25 listed ingredients?  There is nothing about these that actually looks like food.

Essentially, the more it has to be processed before it gets on the supermarket shelf, the less you should be inclined to buy it.  And there is a simple way of expressing this:  Imagine your great, great grandmother is still alive and just suppose she is accompanying you on your next trip to the supermarket.  The rule is then that you can only put something in your shopping trolley if she would recognise it as food.  No soya mince, no chicken nuggets, no breakfast biscuits, no Quorn sausages, no ‘Heart Healthy’ muesli, no margarines.  Only good natural foods would get past the watchful gaze of your dear great, great grandmother.  In fact, I am pretty sure that three quarters of the aisles in my local supermarket would be out of bounds in the hunt for food that actually looks like food. 

Remember too that once it is in your shopping trolley, you will eat it.  The gateway is therefore the decisions you make in the supermarket.   Imagine great great granny and her beady eyes and I am sure you will then make some healthier food shopping choices.

3. If an ingredient is unpronounceable, it is probably indigestible

If it is a packet food, look carefully at the list of ingredients.  I have a rule that I rarely buy anything with more than five ingredients.  More importantly though, if I cannot pronounce any of the ingredients then it is not going to find a space in my trolley.  Microparticularized whey protein-derived fat substitute, anyone?  Potassium metabisulfite perhaps?  Tertiary butylhydroquinone (TBHQ) maybe?  Double helpings of Dioctyl sodium sulfosuccinate? Not in month of Sundays and so it should be for you too.

4. Cut the carbs, not the fat and not the protein

From my previous articles you will have read that a big driver in my dietary journey is to minimise the impact of insulin swings in my body’s biochemistry. That is because an impaired insulin mechanism is correlated with so many of the chronic non-communicable conditions of the twenty first century.  And the way to stop insulin swings is to stop eating food that causes spikes in blood sugar levels.

So don’t look at the calorie content of a food, look at the carb content and within that, the sugar content.  My simple rule is that if there are more than 5 grams of sugar per 100 grams of the food, then it is not going in the shopping trolley.  No compromise.  I will then look at the carbohydrate line, if this is more than 10 grams per 100 grams, then that is going to stay on the shelf too.  Those two rules are quite strict and will eliminate much from the standard British diet, but the kindness you will be showing your metabolism by sticking to those rules will be immense.

5. Your fat should be natural, your fibre should be green and your protein should be complete

This is one of the main reasons processed food is so bad for us – manufacturers will use the cheapest ingredients wherever they can to cut costs and improve profit margins.  The sources of fat, fibre and protein in processed foods will be the cheapest, easiest to manufacture and almost inevitably therefore of the lowest quality. Many are actually harmful to us.

Do not be fooled by a margarine that claims to lower your cholesterol. Cholesterol levels in your blood are only very poorly correlated with health outcomes.  In fact, for the over-fifties, the more of the high density liposome (HDL) cholesterol-carrying molecule in your blood (what is often termed as your ‘good cholesterol’), the better your health outcomes will be.  Margarines actually lower this ‘good cholesterol’.  

Vegetable oils, seed oils and many nut oils are bad news too.  Yes, they are cheap to produce, but they have to be chemically extracted, often artificially coloured and flavoured and then further processed to make them stable.  The chemicals used to extract them are bad news for you.  The processing to make them stable is even more bad news for us – the resultant oils are linked to cancer, heart disease, Alzheimers and diabetes. And because of their source, they are high in inflammatory omega 6 fatty acids.  A cocktail of disaster.

Look for oils that are ‘raw’ and ‘cold-pressed’ as these are the ones that are naturally sourced and do not need to be chemically extracted.  Cook with coconut oil, avocado nut oil or lard. Low temperature cooking with extra virgin olive oil, butter and ghee is fine too.  Beware too that not all olive oils are equal – the cold pressed, extra virgin sort is great news.  But, in order to make more profits, oil producers are likely to chemically process the olives to get even more oil out of them.  Olive oil that is just labelled as olive oil (rather than the extra virgin sort) is probably high in the oils resulting from chemical extraction.

If the food you are contemplating has a label, namely a list of ingredients, then you need to look at the list of fats and oils like a hawk.  Shun any food that has vegetable oils or seed oils listed on the label.  As a specific example, shop-bought mayonnaise is very tricky.  Even the leading brand will use cheap, chemically derived and stabilised oils.  You can get mayo made with extra virgin olive oil or avocado nut oil but you have to hunt it down, as it will be the lonely few jars hidden at the back of the top shelf. Better still, make your own.

There has been a strong movement for ‘whole grain’ foods, foods which include the husk of grain and cereals.  Whilst I shall save the detailed discussion of inflammatory lectins to a separate article, suffice to say here that there was a very good reason why we historically removed the husk of grains before eating.  Yes, the husk has lots of fibre but it also has lots of the defence chemicals a plant recruits to stop it being eaten.  These inflammatory chemicals are the evolved weapon of choice in the battle between plants and animals and if we eat them in quantity, the systemic inflammation they cause is significant.  So rather than eat husks for fibre, go to the leafy green vegetables – fibre aplenty but fewer inflammatory lectins.  To make sure that the green fibre you are eating is not sneaking starches and sugars into your diet, there is a fairly simple rule that you should stick to the parts of the vegetables that grow above ground rather than the bits below. The leaves of rocket, kale, spinach are good fibre and low in starches; the tubers and bulbs of potatoes, carrots and parsnips are full of starches and should be limited.  Not an infallible rule, but a good starting point.

Not all proteins are the same.  The amino acid building blocks of protein come in a number of different varieties and whilst all forms of protein have a variety of these amino acids, only animal and fish based proteins have all the amino acids in the right combinations: Humans will find the protein building blocks most closely aligned to their needs in the flesh of animals metabolically closest to humans. The proteins in beans and pulses are a long way down the evolutionary ladder and very unlike our own.  A soya bean and a human a so far apart on the evolutionary tree, that it is unreasonable to expect that there is anything metabolically similar between us.  The way a soya bean makes, uses and stores protein for example will be very different from how Homo sapiensdoes any of these things.  A cow is much closer to us on the evolutionary tree and so its metabolism is more similar to our own.  A mouthful of cow protein is much closer to what we metabolically need than a mouthful of soya protein. 

To use an analogy, it is a bit like taking a modern electric Tesla car to a garage and only having the parts from an ancient Ford Model-T to fix it.  With a lot of effort and compromise you might be able to cobble together a repair but only enough for the Tesla to limp-on.  But if you had parts from last year’s Tesla model instead, you might not even notice the repair.  So don’t rely on plant based proteins if you want to have optimal animal protein nutrition.

6. If it’s in a packet, don’t snack it!

A recent study conducted in the United States suggested that a third of all of Americans have fifteen or more ‘eating events’ a day.  An eating event includes a drink with calories (milky sugared tea or coffee, for example) as well as food, but nonetheless consuming calories in fifteen separate occasions each day is grazing gone mad.  Cows graze because they need to; we do not.

If you do need to snack, can I suggest a few ‘rules’ to reduce the urge?  If you are going to snack during the day, first thing in the morning put the entirety of the food you plan to snack on in a dish. So if you are going to have biscuits (but please try not to), put two in the dish.  If you are going to have some healthier nuts, put a measured portion in the dish.  If you are going to nibble on some cheese, put a cut lump in the dish.  The psychology here is that if you get the urge to snack and your hand dives into a full packet of nuts, cheese or biscuits, one handful of nuts can quickly become two or three and one small lump of cheese can become a slab!  If instead you can see that there are only a dozen nuts in your pre-measured dish and if you take them all now, there will be none for later, you might think twice about the size of the current handful or whether you might leave it and wait until later.

I also have a little armoury of snacks that need preparation – that is they are not available in a packet.  There is for example a low-carb muffin recipe that takes between 5 and 10 minutes to prepare. That then becomes a real test of whether you are actually hungry.  If you cannot be bothered to spend 10 minutes making the snack, then you obviously don’t really need it.  It is all too easy to reach inside a packet for something to snack on but if you have to spend time making it, you will only do that if you really need the calories. 

In my next article I will take a look at cholesterol, a word that seems to stir so much fear when it comes to nutrition and yet is a substance so vital to us.  ‘A Spoonful of Medicine Helps the Sugar Go Down’ will examine how we have got it so very wrong.

To read this next article click here

To read the previous article click here

Phil Nuttridge continues his series of articles looking at the modern take on diet and nutrition.  He explodes many of the dietary myths that have 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 insulin’s role in obesity, diabetes, heart disease and inflammation.  More information can be found on Phil’s website cuttingcarbs.co.uk or by following him on Instagram:  CuttingCarbsUK

Maybe it is genes, may be it is lifestyle choices.  Whichever it is, I am very fortunate:  At 53 years old, I have a BMI of a little under 23 and I am no more than nine percent body fat.  Not bad stats for an “old ‘un”!  But this has not always been the case – there was a time in my life when I was quite the little porker.  You could definitely pinch more than an inch anywhere and everywhere on my body.  At the time though, everyone was rejoicing in that chubbiness and that’s because it was when I was born.  I was a (very) big and bouncing baby!

It probably hasn’t escaped your notice that most of us are chubby at birth.  In fact, new-born human babies can be upwards of fifteen per cent body fat.   What is intriguing is that this is unique to Homo sapiens as we are the fattest babies in the animal kingdom and by quite a margin.  The new-borns of our closest primate cousins do not make it into double-digit percentage body fats; even mammals we think of as fat, like seals, piglets and puppies, are rarely more than ten per cent fat at birth.

Carrying an extra-fat baby to term places huge energy demands on the pregnant mother.  Taking the view that this is not just an ‘accident’ of Nature but rather a response to an evolutionary pressure, what survival advantage could this confer to human babies?  Well, nutritional anthropology seems to have the answer and it all centres around the most energy demanding organ in our body – our brain.

Humans are big-brained and this is a trait that has helped us become the apex species on Earth.  But at what stage in our development do we grow our large brains?  If we grew our brains in the womb, this would require our mothers to  develop wider hips to allow safe birthing.  But wide-hipped bi-pedal humans are not good runners, bad news for a hunter-gatherer apex species.  So, evolution has developed a clever solution to the problem:  In the womb, the human brain develops to just a moderate size compared to the rest of the baby.  Additionally the in-the-womb human baby is ‘packaged’ with the energy store and building material that enables it to crack-on growing a bigger brain after birth without having to wait for its eating habits to develop.  Those energy and material stores are the rolls of chubbiness we are born with.

The clever thing for our nutritional journey is just how the baby becomes fat.  It uses the same metabolic mechanism that (for example) bears use to pile-on the pounds just before Winter hibernation.  That mechanism is reversible Insulin Resistance.  Regrettably, as I shall show you, in the last fifty years this mechanism has back-fired on us humans and provides an eloquent explanation for the epidemics of obesity and Type II diabetes in the modern age.  More of that later but firstly, I need to talk about insulin and what happens when we become resistant to it.

Insulin is the key hormone for lowering excess blood sugar levels in the body.  When we have eaten a meal containing sugar or starch, the latter of which is broken down into sugar by our digestive enzymes, then sugar molecules (principally in the form of glucose) will be absorbed into our blood raising our blood sugar level.  Short term this is fine, but our body does not like too much sugar in the blood for too long as these pesky glucose molecules just love attaching themselves to any and every protein molecule they can find.  Proteins are fundamental to the chemistry, structure and function of our body cells – they form enzymes (the catalysts that facilitate chemical reactions), hormones, antibodies, transport molecules like haemoglobin, collagen and muscle fibres.  But a glycolated protein, one that has been attacked by glucose, cannot do its designated job properly: Sugar with protein is bad news!

Glycolated proteins are bad news on another front too.  Because they are ‘mongrel’ molecules not naturally found in the body, our immune system is likely to identify them as foreign invaders.  Immune responses are triggered potentially leading to auto-immune disease and inflammation.  Very bad news for our body.

To overcome this we have evolved clever chemistry to keep our blood sugar levels in check.  The hypothalamus in our brain constantly monitors the concentration of sugar in the blood and if the level rises above a threshold value, signals are sent to the pancreas to release the hormone insulin.  Insulin acts quickly and sets things in motion to get that extra sugar out of our blood.  

Different parts of the body listen to insulin in different ways.  In summary though, insulin mediates a metabolic switch:  One setting of this switch, the way it is set in the absence of insulin, tells our body to give-up its fat reserves and use them for energy; the other side of the switch, triggered when insulin is circulating, tells our body to bolster its fat reserves and preferentially use sugar for energy.  

How does insulin operate this switch?  Well, it has a number of actions all of which combine to give this effect:

1. Insulin controls entry of glucose into your muscle and fat cells.   When insulin is present, important transport mechanisms in cell membranes open-up and allow glucose into the cells.  This is key for insulin’s role in reducing blood sugar levels – open the cell doors and glucose will pass out of our blood and into those cells, thereby naturally reducing blood sugar.  Significantly, the liver and brain cells which have high demands for energy do not need insulin for glucose to enter as they have transport mechanisms that are insulin independent.  
2. Insulin tells the liver to stop producing glucose and start producing glycogen.  Our liver is very good at making glucose from fats and proteins.  In fact, because of this gluco-neogenesis, all the glucose needs of our body can be met from fat and protein and consequently there is no minimum daily requirement for eating carbohydrate.  The same is not true for fat and protein.  Although the liver can make a lot of protein and fat building blocks, not all can be made and so our diet must contain these ‘essential’ fat and protein components.  Our health will quickly fail if we stop eating protein and fat yet we will survive, even thrive, if we cut our carbohydrate intake.  Our liver naturally pumps away producing glucose but this process stops as soon as insulin is detected.  Instead, the liver switches to converting blood glucose into glycogen, a storage form of glucose, that takes glucose out of harms way and stores it as a ‘banked’ fuel for later.
3. Insulin tells the liver to make triglycerides.  The body can only bank so much glycogen.  After this limit is reached any further glucose is then converted to fatty acids and triglycerides destined for storage in the skin.  And these are the real bad guys.  Although I will save my demolition of the ‘cholesterol is bad’ fallacy to a later article, let me say at this stage that the blood measure that IS correlated to worsened cardiovascular outcomes, is blood triglyceride level.  The higher blood triglyceride, the more the chance of developing cardiovascular disease.  And those triglycerides come from insulin-mediated processing of excess sugar.
4. Insulin inhibits the breakdown and metabolic use of adipose fat.  The adipose fat is the fat that lines the skin.  It is the fat that makes us look fat.  When there is too much sugar around, insulin tells the body to stop burning fat for energy and use sugar instead.  Under the control of insulin, the pathways that mobilise fat and use it for energy cease and instead the body goes full-on into the mode of deriving energy from sugar and converting any excess sugar to storage fat.  

Insulin therefore tells our cells to cling on to our fat reserves and add to them if there are excess carbs around.  You can see that if you want to lose weight and be healthy, then ideally you need to eat minimal amounts of the food that trigger insulin:  You need to eat fewer carbs.  That clipperty-clop sound you can hear right now is my hobby-horse trotting off into the sunset!

One other point to make here is that insulin also has an anabolic effect on the body in that it mediates tissue growth and replacement.  Insulin telling the fat cells in our skin to take-up glucose in order to make bigger adipose reserves is one example of this anabolic function.  Other anabolic pathways controlled by insulin include the production and uptake of structural proteins, the expression of genes and the replication of DNA all essential for tissue regeneration and growth.  Of course we need this and so some insulin is essential.  However, too much insulin too often will over-stimulate these anabolic functions and excessive cellular regeneration, unchecked, leads to uncontrolled cell proliferation, the bedrock of cancer.  Even non-malignant proliferation can be problematical if those tissues are for example, our fat cells or the cells lining your blood vessels.  The perfect storm of inflammation and cell proliferation – both caused by excess insulin – can lead to atherosclerosis, the thickening of blood vessel walls and a precursor to heart disease.  They used to think that eating too much fat thickened our artery walls but now we know that it is from excess carb-triggered insulin.

The recurring message here is that for good health outcomes we need to control our insulin levels – we need to avoid producing too much too often.  

Compounding this problem, the insulin mechanism is itself under attack if we follow a diet perpetually consuming large amounts of starch and sugar.  The  persistent triggering of insulin to deal with the daily spikes in blood sugar levels begins to takes it toll.  The insulin receptors on the cell membranes of the target cells start needing higher concentrations of insulin in order to be triggered.  We could say they start becoming partially deaf to the insulin message.  This is the start of Insulin Resistance.  Insulin Resistance then sets up a vicious and escalating cycle:  If the insulin receptors become a little ‘hard-of-hearing’, the pancreas will respond by releasing a bit more insulin into the blood to get its message across.  But these higher levels of insulin sustained over a period of time will make the receptors even more deaf.  So the pancreas has to release yet more insulin to get its message ‘out there’.  In this ever escalating sequence, eventually the pancreas will no longer be able to release enough insulin to get its message across to all the target organs – the receptors have become just a little too deaf.  This is Type II Diabetes.  Once this condition has developed the body is no longer able to control the spikes in blood sugar brought about by the sugars and starches in the diet.  Those glycolated proteins we met early can now go on the rampage!

Research also shows that not all of the insulin receptors and not all of the pathways from each receptor become equally deaf to insulin.  If we have fatty liver disease for example, then it is likely that the liver becomes deaf to the insulin message rather quickly.  This is very bad news.  Remember how through the process of gluco-neogenesis the liver pumps out glucose when it thinks the body needs it?  Normally the insulin message will tell the liver to stop doing this but if the liver has become deaf to insulin, it will continue to pump out glucose even though there is already raised glucose in the blood (the event that triggered the insulin in the first place).  Blood sugar therefore goes up and not down.  But, and it does seem to depend on your genetic disposition, many of us have fat skin cells that only very slowly become deaf to the insulin message.  You will recall that insulin tells these fat cells to mop-up blood glucose and convert it to fat for storage and avoid burning it for energy.  If the skin cells remain sensitive to every drop of insulin in circulation, then they will go into overdrive adding to their fat reserves because of the excess insulin triggered by a resistant liver.  This is the metabolic pathway to obesity.

Just stepping aside of the argument here, this fits very nicely into my hobby horse that calorie counting is not enough to manage weight loss.  Our insulin model and particularly the model of how with partial insulin resistance our skin fat cells are listening to an overloaded message of insulin to store fat, shows that weight gain is very much under hormonal control.  And because insulin is the hormone in control, how much weight you gain is dependent on the sugar and starch in your diet.

Continuing with our insulin resistance story, you may remember that some of the functions of insulin are anabolic – they stimulate cell growth and proliferation.  Good in small measure but not so good in excess.  This anabolic pathway in the insulin receptors is less likely to become insulin resistant than the glucose absorbing pathway.  So, in a body experiencing rising surges of insulin, those anabolic pathways, just like the skin fat cells, are listening to every drop of insulin.  Cell proliferation, atherosclerosis and inflammation, all triggered by the anabolic functions of insulin, become rife.  

You can now see that excess insulin is not a good thing.  Obesity, type II diabetes, inflammation, cancer, atherosclerosis are all the long term consequences.  Notice how this list is the rogue’s gallery of non-communicable chronic diseases prevalent in the 21st century, all mediated by insulin resistance in turn triggered by regular excess sugars and starches in your diet.  It doesn’t stop there as insulin is an antagonist to leptin, the hormone we met in my last article that tells us when we are full.   An Insulin resistant metabolism that throws large amounts of insulin into your blood will therefore depress levels of leptin and thereby suppress one of the key signals that you are full.  A high carb diet = High insulin = Low leptin = Always hungry.  Insulin Resistance seems to be our enemy.

But here’s the thing.  Becoming insulin resistant has been an advantage to us in our evolutionary past.  This takes me back to our fat babies.

It seems that during the third trimester of the pregnancy, the human baby flicks the insulin resistance switch and becomes temporarily insulin resistant.  It starts to pile-on the pounds of fat and by the time the baby is born we have the perfect fat baby.  But, and this is key, the insulin resistance switch is reversible; once the baby is born, it flicks the switch back and normal metabolism is restored.   So, having a metabolism that can become insulin resistant has served Homo sapiens well in the past.  It has also probably helped us through the odd ice age too.  As times have become tough for humans when ice ages approach, we have probably had to rely more on starch reserves in underground vegetables for energy.  If consuming these in quantity makes us pile on the pounds of fat (through insulin resistance) those pounds of fat have almost certainly made our survival of the cold more likely.  Evolution will therefore have placed a selective advantage on those with the insulin resistance genes.  

To a limited extent this continued to be a survival advantage up until our very recent history.  Each Winter there would be a survival advantage to those carrying a few extra pounds of subcutaneous fat – an extra layer of protective warmth.  How clever would it be if we could trigger piling on a few pounds in the Autumn in readiness for the approaching Winter.  

Until the era of supermarkets and the removal of seasonality of foods, humans would only have had access to significant amounts of sugar and starch in the Autumn in the form of fruits, berries and starchy root vegetables.  Consuming these in the Autumn glut would temporarily overload our insulin mechanisms triggering mild insulin resistance in turn promoting our skin cells to store more fat.  We therefore get those few extra pounds of insulating body fat in readiness for the upcoming Winter.  The key thing though for our evolution is that we then stop eating those sugars and starches at the end of Autumn because they are no longer available.  Our insulin mechanisms restore to normal function, insulin levels fall allowing us to mobilise and metabolise those fat reserves and enabling us to live off them during the Winter.  But modern 21st century Man lives in a perpetual Autumn as starch and sugar are available year-round causing perpetual insulin resistance to obesity.  What once gave us a survival advantage has now turned against us.

Next month, in my article entitled How to “Phil” Your Plate, I shall take a side-step from the modern science of nutrition and talk a little about the practicalities of feeding ourselves in a way that manages insulin and leptin.   Click here to read this article

To read the previous article click here

Below is a copy of my article published in the September issue of Pampering Times.

Phil Nuttridge continues his series of articles looking at the modern take on diet and nutrition.  He explodes many of the dietary myths that have 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 the evidence that calorie counting is a flawed strategy for weight loss and that it is controlled by hormones after all.  More information can be found on Phil’s website cuttingcarbs.co.uk or by following him on Instagram:  CuttingCarbsUK

It is incredibly difficult to make a fat mouse.  If it was as difficult in humans as it is in mice, people like me would not be writing articles like this!

Although there are many ethical arguments against experimentation on animals, obesity experiments on humans are hugely problematical.  So, regrettably, in order to understand better human obesity our little rodent friends are the ones under the microscope.

But there is that first significant hurdle – to study obesity in mice you have to have obese mice.  And that is quite challenging.  Unlike humans we can’t just give them unlimited access to convenience food, a comfy sofa and a Netflix subscription and watch the pounds pile on.

Under normal conditions (and access only to normal ‘mouse food’), laboratory mice are very good at controlling their weight.  If you make excess food available to them, they just eat what they need and leave the rest.  If you reduce food available to them, their metabolic rates reduce to compensate.  If you dilute the energy content of the food they eat, they eat just the right extra amount to compensate.  They do not need calorie counting to keep their weight in order.

Luckily for our experiments though, there are two possible ways to make a fat mouse: 

1. Genetic manipulation
2. Addict them to sugar or foods high in synthetic fats.

Even the second of these is not a guaranteed way of making them fat as sugar-addicted obesity in mice seems to be controllable with faecal implants.  I will come back to faeces later. 

Taking the genetics first, there are two known variants of fat mice, named Ob and Db. Whilst both types of obese mouse look the same, the thing that sets them apart is what happens when we ‘mix’ these mice with non-obese mice.   Regrettably, ‘mix’ in this context is not for the faint hearted.  By ‘mixing’ I mean parabiosis, the surgical procedure whereby two mice are stitched together so that their blood circulations intermix – a bit like the opposite of separating Siamese twins.  Such methods would be frowned upon nowadays, but in the Sixties when these experiments were performed, it was an accepted procedure.

Three parabiosis combinations were investigated and these are summarised below with their results:

Food was not restricted nor exercise imposed in any of these experiments – there was no enforced calorie counting.  Instead, weight loss resulted from something blood-borne passing between the ‘mixed’ mice.   

Where am I going with this?  Well, you may remember the Swearing Gym Bunnies (SGBs) we met in my last article.  We saw that they are the new breed of ‘expert’ telling us the sole reason we are fat is because we do not count our calories.  The SGBs assure us that weight loss is just a simple matter of making sure you burn more calories than you eat.  “Be in caloric deficit” is their mantra, i.e. eat fewer calories than you burn.  Count your calories and you can count on weight loss.  They assure their followers that if you do not lose weight it can only be because you are not tracking your calories properly – you are either eating more than you claim or exercising less than you claim and probably both! 

The mice in our parabiosis experiments did not have SGBs shouting at them to count their calories, instead the mice lost weight because of something being transmitted in the mixed blood.  It took a few decades of research to isolate what this ‘something’ was, but we now know enough of the chemistry to interpret those landmark experiments.

The Ob mouse was missing a factor in its blood that told it when to stop eating because it was full – the Ob mouse got fat because nothing was telling it when to stop eating.  The normal thin mouse had this factor in its blood and so knew when it was full.   When in Experiment 1 the two were mixed, the factor from the normal mouse was passed into the Ob mouse. It then had the factor telling it when to stop eating and so it lost weight.

The Db mouse’s story is a bit more interesting.  It turns out this mouse not only had the ‘stop eating’ factor circulating in its blood, it actually had rather a lot of it.  What had gone wrong in the Db mouse was that its brain was deaf to the ‘stop eating’ message.  The bit of the mouse that produced this factor was shouting its ‘stop eating’ message ever louder but it was not being heard, hence the elevated levels of the factor.  This was bad news for the normal mouse that got mixed with it in Experiment 2.  The excess ‘stop eating’ factor passed into the normal mouse’s blood whose brain listened to the ‘stop eating’ signal all too clearly and kept listening.  This poor thin mouse eventually died of starvation through the unrelenting ‘stop eating’ message.

In Experiment 3, the ‘stop eating’ factor from the Db mouse entered the blood of the Ob mouse, whose brain was still able to listen to the message.  The Ob dramatically lost weight like the normal mouse in Experiment 2 but because it had more fat reserves, it lasted rather longer. 

This factor turns out to be the hormone leptin that we met in my last article, the hormone released by the fat cells in our skin once they have received enough fat.  Ob mice fail to produce leptin and Db mice produce leptin but instead their genetic fault leads to leptin resistance in the brain: No matter how much leptin you throw at it, it will not listen to the ‘stop eating’ message.

We now know that the human mechanisms controlling obesity are very similar to those in a mouse – we too have leptin.  Just like the Ob mice, there is a rare genetic disorder in humans that prevents our fat cells producing leptin causing insatiable hunger and obesity.  This human condition has been successfully treated with leptin injections.  Humans can also suppress the production of leptin with bad dietary choices – rapid weight loss through calorie restriction being one of those bad choices.  If you attempt weight reduction through eating fewer calories and those calories are high in carbs and synthetic fats, then your ‘stop eating’ signal gets quieter and quieter.  You rely on willpower alone to stop eating and when that runs out, the midnight munchies kick in!   Sneakily, the lower levels of leptin also slow down your metabolic processes so that the calories you expend both resting and in exercise reduce.  Your balance between calories eaten and calories burnt moves away from deficit towards balance, taking you out of caloric deficit and into caloric surplus even though you continue to suppress your calorie intake.  Life on reduced leptin is just not fair.

Humans can develop leptin resistance too, though unlike the Db mice in these experiments, human leptin resistance can also be developed through bad dietary choices.  On the plus side, it seems that diet-induced leptin resistance in humans can be reversed at least partly.

Let’s now turn to the second way to make mice fat – sugar and faeces.  Not all mice will become obese if given unlimited sugary and fatty foods but some do.  It is probably of no surprise to you that sugar addiction is a contributor to obesity in mice as it is in humans but did you know mice can find sugar even more addictive than cocaine?  That aside, what about the faeces?

Let me take a moment to talk about microbes.  It is estimated that in a typical adult human there are around 35-40 trillion human cells.  Whilst that is a very big number, what I find even more remarkable is that there are at least as many microbial cells (bacteria, fungi, virus) within each one of us too.  Some estimates put the ratio of microbial cells to human cells at 3:1 or greater.  Whatever the ratio, the entity that you think of as ‘you’ is at least half microbial!

Many of these microbes sit in your gut and we are now learning just how transformational they are in our relationship with food.  To understand this I am afraid our rodent friends are back in the firing line.  

One thing that works in our favour when we study mice is that mice will actually eat their own faeces.  It even has a posh name – coprophagia.  It is an evolutionary strategy that enables mice to absorb vitamin B12 and folic acid released from food by their gut bacteria but too late in the digestion process to be absorbed ‘first time around’.  So, by eating their faeces, the B12 and folic acid released from the first-time processing in the gut then get absorbed in this second pass through.   The consumed faeces will also contain a sample of their gut microbes.  If the faeces are from another mouse, then the ingesting mouse gets exposed to the gut bacteria of the ‘donor’ mouse. 

Remember I mentioned earlier that not all mice get fat when sugar is made available to them.  Here’s the interesting thing: If you take the faeces from one of these thin mice and feed them to a mouse that would otherwise get fat, then the potentially fat mouse remains thin.  The gut microbes of the thin mouse seem to make a pivotal difference.

Interesting corroboration of this for humans comes from the study of twins.  Studying identical twins reduces the effect of genetic variation in any analysis as the siblings have an identical genetic make-up.  What is useful is if you can find sets of such twins where one of the siblings is of normal weight and one is overweight or obese.  Fortunately sufficient instances of such twins have been found and studied.  It is particularly interesting when we look at the diversity of the gut microbes in each twin.  Consistently, each normal weight twin has a much greater diversity of gut microbes than their over-weight or obese sibling.  

Inconveniently (from a research perspective), we humans do not have a penchant for eating faeces!  Instead, experiments of surgical faecal transplantation between thin and obese humans are showing similar results to the mice experiments.

So, what you eat matters because food groups can alter leptin production and leptin sensitivity.  Your gut bacteria matter too.  I think the SGBs would start swearing at me if they heard that.

Let me now anticipate an objection here:  Surely it is just mind over matter – with enough willpower (being shouted at by SGBs, for example) surely we can overcome the limitations leptin imposes on calorie restriction?  Fortunately there is some (old) research that helps answer that very question.

One of the big problems with human food research is the ethics of strictly controlling exactly what a group people eat and do for a sufficiently long period of time to have a meaningful and measurable effect.   (Un)fortunately during the Second World War, some researchers had access to a group of people who could have their diet and exercise very rigorously controlled – imprisoned Conscientious Objectors.

Now referred to as the “1944 Minnesota Starvation study”, this experiment placed a group of Conscientious Objectors on a strict diet of reduced calories and enforced exercise.  Of course, this is exactly what the SGBs tell us to do but the 1944 study enforced things to a degree no SGB could ever hope for. 

In the first weeks of caloric deficit, the 1944 test subjects duly lost weight.  One – nil to the SGBs.  The thing is though, this weight loss did not continue as planned.  The rate of weight loss reduced as the experiment progressed; even though the subjects were on the same calorie restriction and the same levels of enforced exercise – in other words, their caloric deficit was being maintained – they stopped losing weight.  Some even started to regain weight.

Our calorie counting SGBs will tell us that cannot be – stay in calorie deficit and you will continue to lose weight.  If the SGBs had been at the helm of this experiment they would have been shouting and swearing, claiming that the subjects were not losing weight because they were lying and cheating; they were being glutinous and/or lazy.  But the Minnesota experiment showed otherwise.  The subjects’ calorie intakes WERE rigorously controlled (no opportunity for cheating there) and they WERE forced to continue with the exercise regimen (no cheating there either).  In fact, in order for weight loss to be achieved and maintained for the whole of the starvation phase, calorie intakes in the study were repeatedly reduced so by the end of the trial some participants were on fewer than 800 calories each day.

That this was leptin’s revenge is evidenced by the behaviour and mood of the subjects.  Despite the starvation phase being conducted in the summer, the participants constantly felt cold.  Their muscular strength reduced by twenty per cent.  Resting heart rates plummeted, some to as low as 35 beats per minute. Cardiac outputs reduced twenty per cent; blood pressure scores lowered too.  They experienced dizziness, lethargy, mania, depression, and anxiety.   The lower leptin levels caused by the calorie restriction meant they were completely lethargic during the non-exercising parts of the day and burning fewer calories than before during their enforced exercise sessions.  They were in such metabolic shut-down that their total calorie expenditure reduced sufficiently to compensate for the lowered calorie intake.  A controlled calorie intake that had started off as caloric deficit became calorie balance, even for some caloric surplus.

When the test subjects were finally put on the recovery phase of the experiment and given freedom to eat and exercise as much or as little as they liked, the subjects dutifully and rapidly put all the weight they had lost back on and in most cases around ten per cent extra too.  Their lowered metabolisms now meant that even eating food at pre-diet levels caused significant caloric surplus and therefore rapid weight gain. Their percentage body fat was also significantly higher after the experiment as their bodies had gained fat in preference to lean body mass in the recovery phase. 

The Minnesota study proved that calorie deficit only works in the short term.  Leave it long enough and leptin-controlled responses bring about metabolic reduction to restore caloric balance.  Leptin changes also attack your mood and willpower, eventually forcing us to resume normal eating.  When normal eating is restored, the reduced metabolism leads to rapid weight gain because of the now caloric surplus.  The yo-yo diet is born!

To summarise, the two rules of all calorie restricted diets:

1: All diets work

2: All diets fail

Initially the diet works – better eating in terms of quantity and quality of food will give you weight loss.  Eventually though the body fights back and returns you to where you started through altered metabolism and reduced willpower.  Your body does not like change.   

But if it does not work, why is calorie counting such a part of our psyche?  Maybe it is not too dissimilar to why there are ‘flat-Earthers’ out there.  Look out your window and apart from a few undulations, the Earth undeniably does look flat.  However, physics and global exploration clearly show us that this is no more than a local approximation of a spherical planet. Most people accept that.  If I equate ‘leptin deniers’ (a.k.a. my SGBs) to ‘flat-Earthers’, you can perhaps see my comparison.  Because calorie counting works in the short term, the leptin-deniers extrapolate it as a complete long-term solution too.  It is hard to convince them otherwise as, unlike a few harmless flat-Earthers, the leptin-denying SGBs make a lot of money from their view of the world!

Perhaps I can beat them at their own game.  I could market a ‘STEP ON THE CRACKS IN THE PAVEMENT’ diet.  It would read:  “Rather than eat lunch, go outside and step on the cracks in the pavement for half an hour.  Do that every day and I guarantee in two weeks you WILL have lost weight”.  Ker-ching.  A potential money spinner.  

However, beyond this initial success, as we now know, leptin’s hold will kick-in:  After two weeks, you might spend only fifteen minutes stepping on the cracks in the pavement; you might do it more slowly than at first; you might take a packet of crisps out with you while you are ‘crack-stepping’.  You might dive into a mid-afternoon snack instead. You might have a power-nap in the afternoon to save some calories. Or when you get home, you are slumped on the sofa all evening rather than going to Zumba.  Leptin has a lot of strategies up its sleeve.  As long as I have done a runner by the time this happens and when all the weight has been put back on, I am quids-in with my cunning diet plan.  And so it is for the calorie counting SGBs out there.

Leptin is inevitably just part of the story. In next month’s instalment I will share with you the story of insulin and its role in weight gain – a tale of Ice Ages, Fat Babies and Autumn binges.  

To read the next article click here