England place for Carl

Congratulations to Physicality personal trainer Carl for being selected for the England team to race in the Armagh 5k last week. This is one of the fastest 5k races in the world with 147 runners finishing under 15 minutes! Carl ran 14.11, just a few seconds off his PB.

Core Stability – the basics – 9/7/18

Superman – done correctly

The structure of the skeleton and the generation of movement by muscles is a mechanical issue. So let’s start by looking at the relevant anatomy.


  • Structure of the spine – 7 cervical, 12 thoracic, 5 lumbar vertebrae and the sacrum (4 fused)
  • Natural curves of the spine – kyphosis/lordosis
  • Weight bearing properties (slumped v. neutral spine)
  • Inter-vertebral discs IVD– shock absorbing/ gel like centre – nucleus pulposus/ annulus rings / repeated flexion and extension causing injury. Anyone from mid 30s onwards will have signs of IVD disease (IVDD) – it’s an ageing change. (See gel pack).
  • Movement in 3 planes –sagittal, divides the body in to left and right (actions: flexion/extension)/ frontal, divides the body in to front and back (actions: lateral flexion/extension)/ transverse (action: rotation)
  • Huge increase in compressive forces on IVD with flexion, lateral flexion and rotation – always move your feet to lift an object instead of twisting down to lift it
  • Posture for maximal performance/reduced injury in sport (and life) is a “neutral” spine
  • In order to maintain a “neutral” spine, we need a strong core
  • Hare bones – see how they fit together, where the IVD lies, how the facet joints interlock, where the spinal cord runs through the centre, where the spinal nerves emerge from the inter vertebral foraminae between the bones and how little range of movement the bones have in any of the 3 planes.


  • The body between the thorax and the floor of the pelvis, with the spine running through it
  • Boundaries are the diaphragm at the top, the abdominal muscles around the middle and the pelvic floor muscles and sides of the pelvis at the bottom
  • Stabilisation of the spine is by posture first and muscles second. Good posture allows the forces through the spine to be optimally withstood with minimal muscle involvement. When there are forces on the spine which act to move it from neutral, (eg movement of the limbs) then the muscles “fire up” to keep the spine in neutral and protect the back from injury. So what are the muscles which stabilise the core and where are they?


  • Diaphragm. Moves down in inspiration/up on expiration.
  • Pelvic floor muscles
  • Erector spinae muscles (longissimus/iliocostalis/splenius)– the long muscles running parallel to the spine
  • Deep spinal muscles (interspinalis/semispinalis/spinalis/rotators/multifidus)– closer to the vertebrae and deep, some spanning only 2-4 vertebrae
  • Muscles of the spine play a very important role in stabilising the lumbar vertebrae
  • Abdominal muscles (transversus abdominis or TA/ internal and external abdominal obliques/ rectus abdominis – the “six pack” muscle)
  • TA is like a corset around your middle. It increases intra-abdominal pressure on contraction, which stiffens and stabilises the lumbar spine
  • Trunk muscles (latissimus dorsi/quadratus lumborum/gluteals)

Together these muscles stabilise the core and help maintain a “neutral” spine during movement. This has 2 important consequences:

  1. Prevention of injury. The lumbar spine is mechanically weak. Excessive forces during movement can cause damage. ( IVD, annular rings and delamination under repeated compression /disc herniation/facet joints/muscles especially QL, nerve entrapment)
  2. Improved performance. The core must be stiff to transmit the forces generated by the limbs (tennis players hitting the ball, runners or cyclists transmitting forces through the ground or pedals, sports involving jumping). A weak core dissipates the forces generated and the effect of any movement is reduced, so you run/cycle slower, jump less high or far, hit with less power. Weight lifters generate “super stiffness” by recruiting more motor units within their muscles to enable them to lift heavy weights.

What is different about training core muscles to other muscles?

In the past, training the core muscles has focussed excessively on TA (to increase intra-abdominal pressure and make the spine more rigid) together with repeated flexion/extension from sit-ups/back extensions which create damaging forces on the IVDs. This is applying the same training techniques to the small stabilising muscles of the spine and abdomen as to “prime mover” muscles such as quads and biceps, which move the limbs. Prime mover muscles move through a large range of motion and are “fast twitch” muscles generating a large force over a short time. But core muscles are “slow twitch” endurance muscles which contract steadily for long periods of time and move through a small range of motion or not at all. So unlike training limb muscles, core stability training should focus on very small movements or no movement at all, resisting the forces generated by instability whilst maintaining a neutral spine. The development of core stability enables an athlete to “flow” – to move effortlessly as the core muscles maintain good posture for long periods of time while the big “prime movers” do all the work.

How not to do a “superman” – excessive IVD pressure generated by overextension of the lumbar spine


Fishing rod +/- guy wires

Motor control errors – many back injuries caused by failure of deep, small muscles to “fire” quickly enough as the spine moves eg picking up a pencil from the floor, bending over the sink. Training core muscles involves training the neuromuscular system to activate these small muscles quickly. Balance training is important for this.

Moment arm – the further away from the lumbar spine the object is, the greater the moment arm (15x at arm’s length) and the harder it is for the spinal muscles to stabilise the vertebrae

Eg hoovering/ opening a door/ pushing or pulling an object/holding an object at arm’s length

5 stages of core stability training

  1. Posture – sit/stand/walk with a neutral spine (slump/sit up, shoulders back and down, rotate pelvis to stand tall, walk with arms swinging from shoulders)
  2. Endurance – learn to maintain that posture without the muscles getting tired (see 3 basic core exercises later)
  3. Movement patterns – learn to move from one posture to another whilst maintaining a neutral spine. (squat and lift/lunge/twist/push/pull/balance). Train movement not muscle. Learn to hip hinge (squats/stand from sit/rowing/good mornings/Arabesque).
  4. Strength – increase the ability to keep a stable spine as load increases (more challenging core exercises in the next talk!)
  5. Power – (force x velocity) comes from the hips not the spine. High spinal velocity/low torque OR low spinal velocity/high torque but NEVER high spinal velocity/high torque. The faster your spine moves under load the greater the risk of injury (explosive jumping/throwing).

A note on stretching.

Back flexibility is NOT required for good performance. Flexibility without strength and motor control is useless. In fact the soft tissues of the spine have a passive stiffness and loss of this stiffness by stretching may lead to injury. So:

Don’t stretch your back beyond the range of movement required for competition.

Don’t stretch at all for the first couple of hours in the morning – the IVDs are more turgid with fluid after lying down overnight and are more susceptible to injury.

Don’t do “silly stretches” in which your lower back flexes (usually aimed at the hamstrings).

Lumbar flexion rather than a hamstring stretch

3 BASIC CORE EXERCISES – Superman/side plank/curl ups

 These 3 exercises are described as “The Big Three” by Stuart McGill who is an expert on back pain and rehabilitation of top class athletes with back injuries (see the bibliography).

He advocates these 3 simple exercises which work the core in all 3 planes and develop posture and endurance – the first 2 aspects of core training.

Warm up with the “cat/camel” to decrease the viscosity of the IVDs and reduce the stress on them. This is a motion exercise and not a stretch. Don’t push beyond a comfortable range of motion, move slowly and constantly and repeat it 5-6 times.

Superman  2 x 10

Face down on your hands and knees, back neutral. Slowly lift one arm and the opposite leg (keep them straight) to horizontal and hold it there for a few seconds then return under control. Do not allow your back to leave neutral. Repeat with the other arm and leg. This exercise is all about control – perform it slowly and do not allow your hips to shift side to side.

Side plank 2 x 1 minute (building to 2 minutes) each side.

Side plank support on elbow and feet. Have heel of top foot just in front and contacting the toes of the other foot (not feet on top as in this photo but as below in a slightly more advanced version).

Raise hips off floor and hold. Keep hips forward and squeeze glutes. Do not allow top shoulder to drop forwards. Start with 7-8 second holds at first then increase the number of repetitions i.e. start with repetition rather than duration

Curl ups 2 x 10

Lying on your back with your arms folded across your chest. One knee bent at 90’.Engage your core and slowly lift your shoulders 30 degrees off the floor using your abdominal muscles. DO NOT flex your neck. Lower under control back to the floor.

(Personally I find clients struggle with good technique doing curl ups and find it hard not to engage their neck so an alternative to curl ups would be:

Bent leg lowers 2 x 10. Flat on your back with knees and hips bent to 90 degrees. Maintain your back against your hands (between your lower back and the mat) as you lower both legs to the mat and back to the start position. Do not allow back to lift off your hands. Breathe out as leg goes down and in as it comes back to avoid breath holding.)

Bent leg lowers

These 3 exercises work the core muscles in all 3 planes whilst keeping the back in a safe, neutral position. If you attempt them and are unable to maintain good technique as you tire – STOP.

The second talk on core stability will look at Stages 3, 4 and 5 of core stability training (movement patterns, strength and power) and demonstrate a range of more challenging exercises.


  1. Pocket Atlas of the Moving Body (2000) by Mel Cash
  2. Low Back Disorders (2007) by Stuart McGill PhD
  3. Ultimate Back Fitness and Performance (2009) by Stuart McGill PhD
  4. Strength and Conditioning for Triathlon (2013) by Mark Jarvis
  5. Essentials of Strength Training and Conditioning by Baechle and Earle

General Data Protection Regulation (GDPR) Notice

General Data Protection Regulation (GDPR)

There is new data protection legislation coming in to force in the UK on 25th May 2108. This legislation is the General Data Protection Regulation (GDPR) which replaces the old Data Protection Act. The legislation affects every business that handles personal data for clients. Personal data has been defined by the act as “ any information relating to an identifiable person who can be directly or indirectly identified”. This will include such data as name, address, gender and contact details but also may include information such as IP addresses.

The GDPR includes the following rights for individuals:

  • the right to be informed;
  • the right of access;
  • the right to rectification;
  • the right to erasure;
  • the right to restrict processing;
  • the right to data portability;
  • the right to object;
  • the right not to be subject to automated decision-making including profiling

Fair Processing Notice for Physicality

The personal data we collect about you will include data relating to your name, address, gender, date of birth and wider contact details. We also collect data about your health, medical conditions and any medications. We will use your personal data for the sole purpose of providing the physical therapies of sports/soft tissue massage and/or personal training. We will only use the data for the purpose for which it was collected. We will only share or grant access to your data with a specific third party if you request us to do so.

Your data will also be used to notify you of meetings held at or by Physicality which we feel may be on interest or benefit to you or any special events or promotions for the therapy you participate in. You may opt out of receiving such communications at any time by emailing us at carole@physicality.info.

Record Keeping and the GDPR

Personal data should be kept for no longer than is necessary. It is a condition of both our insurance policies and our membership of a professional body for the exercise profession, the Register of Exercise Professionals (REPS), that we take and retain client records.

The requirements are that these records should be kept for at least 7 years following the last occasion on which treatment was given. In the case of minors, it is advisable that the records should be kept for at least 7 years after they reach the age of 18 years. We will keep client records for as long as we deem necessary rather than 7 years to cover both this professional requirement and the Statute of Limitation for injury claims in the UK.

Full details of our privacy notice can be found on our website www.physicality.info.


GDPR Privacy Notice

Privacy Notice

 Physicality is the trading name for Cycle Tough Ltd trading as Physicality. We are a registered company in England number 09215811. Our registered address for trading is 160, Main Street, North Sunderland, Seahouses, Northumberland NE68 7UA.

This notice is designed to help you understand what kind of information (personal data) we collect in connection with our services and how we will process and use this information. This notice describes how we collect, use, share, retain and safeguard personal data. It also sets out your individual rights.

 What is personal data?

In the context of our business, the personal data we hold on you may include name, address, gender, wider contact details, health parameters (height, weight body mass index etc), medical information, current or past medications and clinical notes relating to soft tissue massage/treatment and/or personal training sessions.

You may provide us with personal data when completing consent forms or questionnaires, contact by telephone or email, writing to us directly or providing us with medical information.

We will not share or grant access to your data to any third party without your specific verbal or written consent unless required to do so by law.

 Why do we need your personal data?

We will use your personal data for the sole purpose of supplying you with the services you have requested, either sports massage/soft tissue therapy or personal training and for no other purpose. We also use your data for the purposes of our financial record keeping.

We have a legitimate interest in informing you of our services and may contact you about educational meetings at Physicality or promotion of our services. You may request to withdraw from such communication at any time by emailing carole@physicality.info.

We will retain your data for a minimum of 10 years after the end of any contractual agreement (10 years after the age of 18 years for a minor). The retention of data is necessary for insurance and professional regulatory body compliance. We retain the right to retain your data for longer if we consider it necessary.

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There are legal rights granted to individuals governing the use of their personal data. These rights allow individuals to understand what personal data relating to them is held, for what purpose, how it is collected and with whom it is shared, where it is located, to object to its processing, to have the data corrected if inaccurate, to take copies of the data and to place restrictions on its processing. Individuals can also request the deletion of their data. These rights are known as Individual Rights under the Data protection Act 2018. These are:

  • the right to be informed;
  • the right of access;
  • the right to rectification;
  • the right to erasure;
  • the right to restrict processing;
  • the right to data portability;
  • the right to object;
  • the right to erasure
  • the right to data portability (receive a copy of your data)

Individuals can exercise their rights at any time. In some situations we may be unable to fully meet your request, for example we may be required to retain clinical records for insurance purposes or financial records for taxation purposes.

 Protecting your data

We will take all appropriate technical and organisational steps to protect the confidentiality of your data (password protected computer in a locked building).

 Contact us

If you wish to contact us regarding any aspect of your personal data or GDPR please email carole@physicality.info


Calories – and why you shouldn’t count them 5/3/18

Do you think calorie controlled diets work?

Do you think all calories are the same?

Do you think people are overweight because they eat too much?

Then think again. Here are the notes from this month’s talk.


CALORIES- and why you should not count them

Everybody has heard of calories. An intake of calories which exceeds the calories expended is the commonly accepted reason for putting on weight, and to a certain extent that is true as energy not used is stored as fat. On this basis, apart from being more active, if you want to lose weight the message is to cut calories e.g.

  • Current drive to restrict children to “100 calorie” snacks only
  • Calorie labelling of supermarket foods
  • Daily recommended calorie intake for adults of 2000 for women and 2500 for men
  • NHS weight loss plan to restrict daily calories to 1400 for women and 1900 for men
  • Diet groups which allow “sins” (cake, desserts etc) as part of a calorie controlled plan
  • 10,000 steps/day

But it’s not as simple as that.

What is a calorie?

A calorie is a unit of energy. Two categories:

  • Small calorie (gram calorie) = the amount of energy needed to raise the temperature of 1 gram of water by 1 degree Celsius at a pressure of 1 atmosphere
  • Large calorie (kilogram calorie, kcal, Calorie, food calorie) = 1000 small calories

The term “calories” in this talk refers to large calories and I’ll use a capital “C”, typos apart.

So, for example, a large banana contains about 100 kcals or 100 Calories.

How do we measure food Calories?

  • Bomb calorimeter – burn food and measure the temperature change in the surrounding water. Rarely used now.
  • Add up the energy content of the macronutrients (fat, carbohydrate, protein) in the food and subtract the fibre (not digested)

1 g fat                 = 9 Calories

1g protein           = 4 Calories

1g carbohydrate = 4 Calories

Calories in/Calories out (the energy balance equation)

 Calories in (food) minus Calories out (energy expenditure) = weight gained/(lost)

This equation is based on the First Law of Thermodynamics, which says that energy is conserved within a system and cannot be lost. In this case, the system is us.

If the energy balance equation is positive, we gain weight.

If the energy balance equation is negative, we lose weight.

If you eat food of any type from any source, if you don’t burn it off by generating heat or exercising or any other form of energy expenditure, you will gain weight.  This is true.

So, according to the energy balance equation, failure to maintain a normal weight implies one of two things;

  • excess Calories in (gluttony) or
  • inadequate Calories out (sloth).

Obesity is due to eating more than the body needs.

Eating less and moving more is the answer to staying lean.

That is the energy balance equation. It is generally accepted as true and incontrovertible.


This is bad news for the 66% of the population who are either overweight or obese, because the energy balance equation also implies that:

Obesity is a behavioural disorder

The blame is on the individual.

Food companies are complicit in this blame – “Calories from sugary food/drink are fine as part of a Calorie controlled diet”

Governments blame obesity on lifestyle – Michelle Obama’s “Eat less, move more” campaign, the NHS weight loss plan based on Calorie restriction etc.

The acceptance of the Calories in/Calories out hypothesis of weight control puts the blame squarely on the individual for poor food and lifestyle choices. Is this so? What does the evidence about the energy balance equation tell us?

Evidence against Calories in/Calories out


1900s – Pima Indians – lean, sinewy, fit hunter-gatherer population until white man took over their territories and fed them meagre government rations of white flour/sugar/canned goods. They got fat, 40% obesity rate, despite being very poor, on the verge of famine and labouring hard

1930s – Hilde Bruch, a German paediatrician who moved to New York in the 1930s, was shocked by the fat American children, two decades before fast food. These children ate excessively, despite medical advice and parental control. She commented: “Many made strenuous efforts to lose weight, practically giving up on living to achieve it.” But maintaining a lower weight involved “living on a continuous semi-starvation diet” and they couldn’t do it. Bruch said of obesity:

“More than in any other illness, the physician is called upon to do a special trick, to make the patient do something – stop eating – after it has already been proved that he cannot do it”

1951 – Italy and Greece – less food per capita than any other European country, 2400 Cals/d compared to 3800 Cals/d in USA. Yet the working classes, especially the women, were fat.

1961 – Trinidad – 1/3rd of women over 25 were obese with an average Calorie intake below 2000/day.

1974 – Chilean slum dwellers, very poor, mostly heavy labourers, of those over 45, 40% of men and 50% of women were obese

2005 – Sao Paulo, Brazil, slum dwellers, women were obese with thin, underweight, stunted children. Did these women really over eat whilst their children were half starved? They were too poor to overeat and too active in hard jobs to exercise more! Surely the “eat less, move more” mantra did not explain the cause of these women’s obesity?


Women’s Health Initiative

A study by the American National Institute of Health in the 1990s.

20,000 women, of which half were obese, were put on a low fat diet, eating 360 Calories/day less than their normal diet. After 8 years, their abdominal fat and waist circumference had increased and they lost on average 2lbs each. If Calories in had reduced by 360/day and 1lb fat = 3500 Calories, they should have lost 36lbs in the first year alone.

New York hospital study

100 obese people were put on a diet of between 800 and 1500 Calories/day for 2 years.

Initially, only twelve lost 20lbs and one lost 40lbs. Only two of the 100 maintained any weight loss at all after 2 years.

Tuft’s Review – an analysis of all diet trials since 1980

Weight loss of 9-10lbs in the first 6 months was followed by all weight being regained.

Pennington biomedical research centre study, USA, the largest obesity institute in the states

800 overweight/obese by an average of 50lbs each at the start, randomly assigned to 4 diets, all under eating by 750 calories/day. They lost 9lbs on average initially but were on average heavier than at the start of the trial by 1 year.

  1. What about exercise and the energy balance equation?

1970s – Stanford University –did a study on 13000 runners. Those with the highest mileage were leaner. But ALL got fatter every year, even those running >40m/week.

Using the energy balance equation, men in their 20s running 20m/week needed to increase their mileage to 60m/week in their 40s to stay lean, while women running 15m/week in their 20s needed to up their mileage to 75m/week by their 40s!

So exercise did not prevent weight gain in these runners.

“Exercise – the miracle cure” report from the Academy of Medical Royal Colleges Feb 2015

30 minutes of moderate exercise, 5 times a week is described as a “miracle cure”, more powerful than drugs for chronic disease, reducing the risk of CV disease, type 2 diabetes, dementia and some cancers by at least 30%. BUT exercise does not promote weight loss.

“It is time to bust the myth of inactivity and obesity – you cannot outrun a bad diet” by Malhotra, Noakes and Finney in the British Journal of Sports Medicine 2015.

This study comments:

  1. exercise levels have changed little over the last 30 years whilst obesity levels have rocketed
  2. up to 40% of those with a normal BMI have metabolic abnormalities associated with obesity (eg high BP, dyslipidaemia, non-alcoholic fatty liver disease, cardiovascular disease)
  3. for every 150 excess Calories of sugar (eg from Coke) the increase in prevalence of type 2 diabetes is 11 times greater than that for an identical 150 Calories from fat or protein, independent of their weight or exercise levels
  4. dietary carbohydrate restriction is the single most effective intervention for reducing all features of metabolic syndrome and should be the first approach in diabetes management
  5. a high fat/low carbohydrate diet induces high rates of fat oxidisation during exercise and is sufficient for most levels of exercise intensity without the need for added carbohydrate.
  6. fat is the ideal fuel for most exercise (Atlantic rowers 2018– lived on a dehydrated meal plus lots of coconut oil)
  7. the “health halo” of legitimising sugary food and drink by associating them with sport is misleading and increases profit at the cost of population health
  8. that weight can be controlled by Calorie counting and that obesity is due to lack of exercise is a false perception and the public health message should instead be on healthy food choices

 Calories in/ Calories out -Conclusion

Increasing calories out by exercise alone does not control weight gain

Restricting calories in fails to achieve long term weight loss.

To quote Hilde Bruch:

“Under eating is not a cure for obesity, just a temporary reduction of a symptom. So if under eating is not a cure, over eating is not the cause”.

The 20 calories/day calculation

Let’s use the energy balance equation to calculate how much we are over eating to gain the 2lbs/year which, on average, we put on (50lbs between ages 25 and 50).

1lb fat = 3500 Calories

So 2lbs fat/year = 7000 Calories

Over 365 days, that’s 7000/365 = 20 Calories/day, roughly

20 Calories/day is equivalent to one bite of a croissant, 3 bites of an apple or 2oz beer i.e. not much!

If we really only over ate by this much, surely cutting down by two bites of a croissant a day when we started to see ourselves getting fat and lose a bit of weight would be easy? So why do we all get fatter with age?

It’s ridiculous to assume that our homeostatic mechanisms cannot cope with a variation in our Calorie intake of less than 1/100th of the daily total OR that when we start to put on weight, a tiny adjustment to our intake isn’t enough to reverse it.

The energy balance equation is true in retrospect – if you eat more then you expend you will gain weight. But this is not an explanation. It’s equivalent to explaining why someone is an alcoholic by saying it’s because they drink too much. So the evidence from observation and research studies shows that restricting Calories in and/or increasing Calories out both fail to prevent weight gain.


Why does calories in/calories out fail to explain our weight gain/loss?

 The energy balance equation makes assumptions that we need to question:

  • Calories in and Calories out are independent variables
  • a Calorie is a Calorie
  1. Dependent and independent variables

The energy balance equation presumes that Calories in and Calories out are independent variables i.e if you alter one, the other is unaffected.

But they are not independent, they depend upon each other. Reduce Calories in and your body will save energy so Calories out falls, and vice versa.

Your main daily energy expenditure is your Basal Metabolic Rate (BMR).

Decreased Caloric intake can reduce BMR by 40%.

Increased Caloric intake can increase BMR by 50%.

Thus weight loss is quick at first on a Calorie controlled diet, then it slows as Calories out fall in response to perceived semi-starvation and the body expends less energy to compensate.

Your body temperature falls, you feel cold, your skin, nail and hair cells multiply more slowly so your skin and hair look dull and lifeless, you are lethargic as your muscle cells are short of energy, your concentration is poor as your brain is short of fuel and you are miserable. Calories out fall because Calories in has fallen. They are dependent variables – alter one and you alter the other. Weight loss slows or stops. Then as you lose the willpower to stay hungry/tired/miserable and go back to eating normally, the weight piles back on faster than ever because your energy expenditure is still spuriously low. This is also known as “yo-yo” dieting.

Calories out is altered by Calories in.

  1. A Calorie is a Calorie – right?

Here’s a quote from the British cycling website article on weight loss this week

“Weight loss is as simple as Calories in versus Calories out…It doesn’t matter what form, fat, carbs or protein, those Calories take, if the balance is negative, you will lose weight.”

This is true.

So it follows that it doesn’t matter whether the Calories in are from fat, carbohydrates or protein, all Calories are the same aren’t they? Wrong.

Here’s a quote from the US Secretary of State for Agriculture on the release of the 2011 US dietary guidelines:

“If folks want to maintain a healthy weight, they have to be sensitive to the Calories in and the Calories out – not every Calorie is the same

In other words, whether you take those Calories in as fat, carbohydrate or protein matters a lot – their metabolism is quite different.

Carbohydrates (flour/sugar/sweets/soft drinks/beer etc) all raise blood glucose rapidly, thus stimulating the release of insulin, which drives fat into the fat cells for storage and reduces the uptake of glucose and fat by the muscles and other cells. Energy expenditure falls. Energy balance is positive. We get fat.

“Carbohydrates drive insulin drives fat storage” (Professor George Cahill from Harvard Medical School).

Fat and protein have a much lesser effect on blood glucose and hence on insulin production. Our muscle and other organ cells have more energy available to them because the fat cells take less in a lower insulin environment. Our energy expenditure rises. Energy balance is negative. We lose weight.

So the type of macronutrients (fat/carbohydrate/protein) we eat as “Calories in” alters our metabolism by altering insulin production and fat storage. Calories in alters Calories out.

  1. Thermic Effect of Food

Fat and protein take more energy to metabolise than carbohydrates. Protein requires 12% more energy to digest than carbohydrates, which is equivalent to 220 Calories/day.  Calories out is higher for the same Calories in from carbohydrates so the energy balance equation is more likely to be negative.Calories in alters Calories out.

  1. Ambient temperature

If the weather is cold, energy expenditure rises as you use more energy to stay warm. You are hungrier and eat more. Calories out alters Calories in.

  1. Exercise

By far the greatest component of calories out is your BMR. Exercise increases your energy expenditure but compared to BMR the % increase is small. Exercise suppresses appetite during and immediately after but then it increases (due to homeostasis) and you will eat more.

Again – you cannot outrun a bad diet. Diet is far more important than exercise for weight loss  (although of course exercise has vast benefits in other ways). Calories out alters Calories in.

  1. Appetite and satiety

Fat and protein both reduce appetite and induce a feeling of satiety (having had enough to eat) compared to carbohydrates, which increase appetite. So Calories in are naturally lower on a low carbohydrate, moderate fat and protein diet compared to the low fat, high carbohydrate diet advised by the NHS and the USDA. Calorie controlled diets are by definition low fat/high carbohydrate (because fat is high Calorie) and they make you hungry!

Calories in alters Calories in.

  1. Insulin resistance

If our diet is carbohydrate based, glucose levels and hence insulin levels are constantly high. Insulin receptors downgrade their sensitivity. More insulin is released to remove glucose from the bloodstream. Fat cells take up more energy and store it as fat, driven by high insulin. Muscle and other cells are deprived of energy and are “hungry”. We are hungry. We eat more (carbohydrate). Glucose and insulin levels rise. Fat cells get fatter. We get fatter and hungrier.

Think of it as a “weight thermostat”. High carbohydrates drive a high insulin level, which resets our weight thermostat to a higher weight – the higher the insulin level the fatter we get.

In contrast, in non insulin resistant people, if they overeat their BMR rises (from 1800 Calories/day to 2700 Calories/day in one study of overfeeding prisoners) to burn off the extra energy as heat and keep their weight at their set weight level.

Due to insulin resistance, our fat cells take up too much energy and our other cells are deprived so we are hungry. We don’t get fat because we overeat, we overeat because we are fat.

Calories in alters both Calories in and Calories out.

  1. Resting Energy Expenditure (REE)

People with insulin resistance can have a reduced REE i.e. they are more efficient at not expending energy, reducing their daily energy requirement by around 200 Calories/day, as their fat-free mass uses fewer Calories. Calories in alters Calories out.


Calories in/ Calories out and the energy balance equation is flawed

Weight gain/loss is not as simple as changing either Calories in or Calories out in isolation.

Counting Calories will not help with weight control and is actually detrimental.

All Calories are NOT the same.

Obesity is not a behavioural failure.

Obesity is a hormonal disorder of fat regulation.

Fat is not an inert energy store, it’s an active body system which is constantly taking in and releasing fat all day long.

Control of fat regulation is hormonal.

Many hormones cause fat release but only insulin causes fat storage.

Obesity is a hormonal imbalance of insulin:

High insulin = fat accumulation

Low insulin = fat release

Dietary carbohydrates and sugars drive insulin drives fat accumulation

Overeating is a symptom not a cause of obesity

Eating less as a cure for obesity fails

Exercise alone is not enough to prevent fat accumulation

Lowering insulin levels is the key to staying lean

So how do we lower insulin levels?

  1. What to eat

Avoid carb-rich foods, starchy foods, sugary foods, soft drinks, beer, sweets etc.

Avoid “low fat” foods which contain sugar to make them palatable eg low fat yoghurts

High quality protein (eg egg, quality meat) raises insulin less than processed meats

Increase your consumption of natural fats and fibre

Eat real food – grass fed meat/fish/seafood/eggs/fruit/vegetables/nuts/seeds

Carbohydrates drive insulin drive weight gain. Avoid them.

  1. When to eat it

Eat at regular intervals if you are hungry.  Don’t bother with breakfast if you’re not hungry. Skip a few meals if you’re not hungry. Do not snack in between meals as this keeps insulin levels higher for longer – better to let insulin levels drop before the next meal. Don’t eat a lot before bedtime.

  1. Stress

Cortisol is the “fight or flight” hormone released in times of stress to enable us to survive a threat. In the short term it raises blood glucose and usually works in opposition to insulin (which lowers it). However, in chronic, long term stress (work/commuting/family issues/illness) cortisol levels are chronically elevated so glucose levels are constantly high – and this leads to constantly elevated insulin levels. Insulin resistance and weight gain follow. High cortisol causes weight gain via high insulin levels (Cushing’s disease). Low cortisol causes weight loss (Addison’s disease).

So stress causes weight gain. Chill.

  1. Sleep

Sleep deprivation is a major cause of stress because it increases cortisol levels.  In 1910, people slept on average 9 hours/day. Now more than 30% of us get less than 6 hours/day and shift workers even less. Sleeping 5-6 hours/day or less is associated with a 50% risk of weight gain. The point at which weight gain starts is less than 7 hours/day. Sleep 7 hours/day or more.

  1. Exercise

Exercise is a short term stressor and the adrenalin and cortisol released in response to physical activity opposes insulin so that the muscles can take up glucose from the blood. Also exercise reduces stress long term, reducing cortisol levels and hence insulin in between exercise sessions and aiding sleep.

Exercise increase builds muscle, increases muscle cell insulin sensitivity and reduces visceral fat. Exercise reduces insulin resistance.

The positive effects of exercise are due to the positive effects on our metabolism, NOT the Calories expended in exercising.

  1. Intermittent fasting

Part of our evolutionary past – of course we didn’t eat 3 meals a day at regular times when we were hunter-gatherers – we ate when food was available. Many meals were missed, often for days. Intermittent fasts of 12-48 hours are very effective at lowering insulin levels and increasing insulin sensitivity. GP advice should be sought before fasting as care is needed if you are diabetic, have other health issues or are training heavily.

Whilst the cause of obesity (and many other metabolic diseases) is indeed poor food and lifestyle choices, the current advice on reducing Calories in by eating less and increasing Calories out by exercising more fails to control weight gain or achieve long term weight loss.

Instead the advice should focus on healthy food choices NOT calories and lifestyle changes which reduce insulin levels.

And finally: Susan Sontag, an American intellectual, said of obesity in 1978:

“Theories that diseases are caused by mental states and can be cured by willpower are always an index of how much is not understood about the physical terrain of a disease”.

 Additional studies etc:

In 2007, Stanford University conducted an “A TO Z Weight Loss Study”.  Subjects were instructed to eat as much fat and protein as they wanted but avoid carbohydrates i.e a high fat, high saturated fat diet. They were compared with those on a low fat, low saturated fat restricted calorie diet. Those who ate mostly fat and protein not only lost more weight, but also other health parameters improved, namely:

  • HDL went up
  • LDL went up
  • Trigycerides went down
  • Blood pressure went down
  • Total cholesterol stayed the same
  • Risk of heart attack decreased

Another Stanford University study compared a high protein diet with a high carbohydrate diet.

Diet 1: 45% protein/35% carbs/ 20% fat – insulin metabolism improved

Diet 2: 60% carbs/20% protein/ 20% fat – insulin metabolism worsened

Evidence for hormonal control of weight includes George Wade’s study of ovariectomised rats in 1970.

Gp1: ovaries removed, free access to food, rapidly obese, activity levels unchanged

Gp 2: ovaries removed, controlled diet, rapidly obese but sedentary

Gp 3: Ovaries removed, given oestrogen, normal weight and activity levels

Conclusion: ovariectomised rats have low oestrogen levels, higher insulin, their fat gets fatter and they overeat to compensate. If calories are restricted as in gp 2, they become sedentary. Oestrogen supplementation keeps the ovariectomised rats a normal weight with normal activity levels. Obesity, appetite and activity levels are hormonally controlled.

Zucker rats: Bred to be clinically obese. These rats stay obese even in the face of starvation, using up their muscles instead for energy. No matter how little these rats are fed, they remain obese to death.

Reading List:

  1. http://www.nhs.uk/Livewell/Goodfood/Pages/the-eatwell-guide.aspx
  2. “The Obesity Code” (2016) by Dr Jason Fung
  3. “Nutrition and Physical Degeneration” (1939) by Weston A Price DDS  with many reprints
  4. “Pure, White and Deadly: The Problem of Sugar” (1972) by Professor John Yudkin
  1. “The Paleo Diet” (2011) by Dr Loren Cordain
  1. “The Paleo Diet for Athletes”  (2012) by Dr Loren Cordain and Joe Friel
  2. “The Case Against Sugar” (2017) by Gary Taubes
  3. “Fat Chance: The Hidden Truth About Sugar, Obesity and Disease” (2014) by Dr Robert Lustig
  4. “Human Evolution, Diet and Health-The Case for Paleolithic Nutrition” (2008) Mark Hines
  5. “It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet” by Malhotra/Noakes/Phinney British Journal of Sports Medicine 23/4/2015
  6. “The Great Cholesterol Myth” (2012) Bowden/Sinatra
  7. “The Primal Blueprint” by Mark Sisson (2012)
  8. “Why We Get Fat and What To Do About It” by Gary Taubes (2012)
  9. “The Great Cholesterol Con” by Dr Malcolm Kendrick (2008)
  10. “Western Diseases: Their Emergence and Prevention” Hugh Trowell and Denis Burkitt (1981)
  1. “Rebuilding the Food Pyramid” by WC Willett and MJ Stampfer (Harvard School of Public Health) Scientific American 288 no 1 (Jan 2003) 64-71
  2. https://www.theverge.com/2015/2/9/8003971/low-fat-dietary-health-goals-bad-science

NB:The above aims to inform so that individuals can make their own dietary choices – it does not constitute dietary advice


Heart Rate Monitoring – why? Monthly talk 5/2/18

Performance testing on the Wattbike

Heart rate monitoring is easy to do, lots of people have a heart rate monitor but what information is it giving you? How do you use this for training, racing and recovery?

Here are the notes from this month’s talk.


 What is heart rate (HR)?

  • 4 cardiac chambers contract in synchronised rhythm
  • ECG trace (and RR interval = time between beats)
  • Pulse – a peripheral representation of HR as blood passes along an artery
  • Take HR at wrist, 2 fingers gently held against thumb side of wrist in line with index finger OR carotid artery in neck below front of ear/angle of jaw
  • Heart rate monitors HRM– wrist or chest strap, detection of HR by colour of skin (wrist) or electrical impulse ( chest strap)
  • Pulse/HR not necessarily the same in abnormal heart rhythms (eg atrial fibrillation AF or dropped beats)
  • Sinus arrhythmia – HR speeds up on breathing in/slows down on breathing out – this is normal

What is a normal resting HR (RHR)?

Resting Heart Rate RHR = the number of times your heart beats per minute at rest

Take either

  • manually before you get up or
  • use a HRM with a RHR function which measures your RHR over the last 4 hours

Normal RHR varies from about 60 – 80, lower in fit people 40 – 50, < 40 for elite athletes

RHR will increase with

  • Stress
  • Lack of sleep
  • Illness
  • Overtraining
  • Dehydration
  • Alcohol

RHR will decrease with

  • Increased CV fitness
  • Some medical conditions (hypothyroidism, Addisons disease, heart dysrythmias)

What is your maximal HR (HRmax)?

Standard formulae predict age related maximal values.

Most well known and easiest is:

HRmax = 220 – age (years)

eg 50 year old has a HRmax of 220-50=170

This formula works well for those under 50. But actual measurements show that older people over 50 in fact have a slightly higher HRmax than this formula predicts so for older people a more accurate formula is:

HRmax = 206.9 – (0.67 x age)

so now our 50 year old has a HRmax of 173, and a 70 year old has a HRmax of 160 (not 150).

For younger people, say 40, the HRmax predicted are equal at 180 and for those under 40 the second formula predicts a HRmax a couple of beats lower.


Age 30 35 40 45 50 55 60 65 70
220-age 190 185 180 175 170 165 160 155 150
206.9-0.67xage 187 183 180 177 173 170 167 163 160

What controls HR?

Autonomic nervous system – think “automatic” ie not under voluntary control

  • Sympathetic nervous system – fight or flight, hormones (adrenalin and cortisol)
  • Parasympathetic nervous system – vagus nerve, neurotransmitters, digestion

What happens to HR during an exercise session?

  • Increased sympathetic activity
  • Exercise pressor reflex (increase in muscle activity and increases in intensity of exercise increase HR up to HRmax with maximum effort level)
  • Cardiovascular drift – as exercise continues for a longer time, SV falls, and HR increases in order to maintain CO. VO2max falls and performance declines. So HR drifts upwards during a long session. Why? Skin cooling theory – as we get hot with exercise, skin takes more blood volume to cool us so blood returning to heart falls, SV falls. Not proven.

What is the long term effect of training on HR?

With training we get improvements in CV fitness:

  • Increased stroke volume (SV
  • Increased heart contractility
  • Increased cardiac output (CO) during exercise

All of these contribute to reduced RHR ( as CO=SVxHR)

  1. HR monitoring for cardiovascular fitness

HR parameters which change as CV fitness improves include

  • Lower RHR (Miguel Indurain, many times TdF winner had a RHR of 33. For most untrained people RHR is about 70).
  • Lower HRmax. An athletes HRmax is around 10bpm lower than that of an untrained person, because their SV is higher.
  • Faster fall in HR as you recover from exercise


Max values (20 year old): VO2 max l/min HR bpm SV mls/beat CO l/min
Sedentary 3.2 200 100 20
Athlete 5.2 190 160 30
  1. HR monitoring for training

So now we know what HR is, how to measure it and how it changes as we exercise. But how do we use HR to tell us how to train? Training is carried out at different levels of intensity – some sessions are easy, some are moderately hard and some are very hard.

How can training intensity can be measured?

  • lactate levels or % of VO2max – difficult to measure outside a lab
  • rate of perceived exertion (RPE) – subjective, depends on how you are feeling that day. Scale is 6-20, aerobic threshold is around 14, LTHR (race pace) is around 16/17, 20 is maximal effort.
  • HR zones – easy to measure/monitor/specific to the individual

HR Zones

Intensity of a training session can be measured by working at a % of HRmax. The different intensity levels are expressed in HR zones, each zone representing a range of HR for that individual. So to identify the HR zones for an individual, we need to either estimate them from formulae OR do a test.

  1. Estimated HR zones – for unfit individuals for whom a maximal effort test is inappropriate, or fit individuals without access to testing. HRmax can be estimated from their age and training zones calculated as a % of HRmax
  2. Sub maximal test eg Wattbike 3 minute test, estimates MMP and LTHR, does not take you to HRmax
  3. Race eg , TT race, 5km run race. A 5km TT race at maximal effort should be done at around 110% of LTHR, a 10km TT (15 minutes) at 107% and a 40km TT (1 hour) at 100%  LTHR.
  4. Maximal effort test for HRmax, MMP and LTHR – only suitable for trained individuals Ramp test on Wattbike Using either of these 2 methods, training zones as a % of HRmax can be identified which are specific to the individual and tell you at what HR you should be exercising for an easy/aerobic/threshold/race at LTHR/above threshold level intensity.

See Carl’s Wattbike Training Zones from a Ramp test done here and his blood lactate curve from Bath University.

Points to note:

  • “recovery” sessions are very, very easy
  • At 60-70% HRmax you are in zone 2, still easy, should be able to have a conversation but will be getting an aerobic training effect, train for 30-45 minutes
  • Training intensity needs to increase significantly to around 85% of HRmax to train aerobic threshold in zone 4
  • Race pace is LTHR at 90% HRmax or zone 5. Sustainable for up to 1 hour in a max effort race. To train at lactate threshold you must train just above and just below this threshold. Intervals are short 2-5 minutes – it’s extremely hard.
  • Zone 5 training at or above LTHR produces the greatest benefits especially for fit individuals
  • Above zone 5 (zone 6 and supramaximal) trains sprinting only.
  • As  intensity levels increase, intervals get shorter

Take home message:

Make easy sessions easier and hard sessions harder and alternate between them.

Don’t train every day at the same moderate level somewhere in zones 2/3.

Only do 2 interval sessions in zone 5 weekly and not on consecutive days.

Don’t spend too much time in zone 4 – it’s tiring and you’ll get stale.

  1. HR monitoring for recovery
  • Training is a progressively increasing stress to which we adapt and get fitter.( Stress increases sympathetic nervous activity and reduces parasympathetic, so HR increases)
  • Improvements to our muscles and CV system occur during recovery. (Rest and sleep increases parasympathetic activity and reduces sympathetic activity, so HR falls)
  • Without adequate recovery we cannot adapt and get more and more tired, leading to overtraining and poor performance
  • Need to find a balance between stress and recovery
  • Monitor recovery with HR changes in the mornings and heart rate variability (HRV)

Morning Warnings

Every morning when you wake, your body “whispers” to you what it can take that day – most of the time we don’t listen. Athletes keep a daily diary to monitor how they feel. Parameters measured include:

  • Stress levels (exercise, work, finances, fear, diet, disease, alcohol, worry)
  • Sleep quality
  • Fatigue
  • Muscle soreness
  • RHR every morning

The first four are scored on a scale of 1 to 7, with 1 being the best (eg 8 hours lovely sleep) and 7 the worst (no sleep at all). If any are 5 or more, that’s a warning.

RHR is scored as number of beats above or below their normal RHR (eg normal RHR of 45, one morning RHR 50, score is 5. If morning RHR is +/- 5 from normal, that’s a warning.

2 warnings – take training easy that day

3 warnings or more – don’t train that day

Also use HR with other parameters rather than alone to tell you how you are eg:

high HR/low RPE or low wattage = not well

low HR/ high RPE or high wattage = fit and well

low HR/high RPE and low wattage = not well

Heart Rate Variability (HRV)- some HRMs only

A measure of stress of any type, including exercise. HRV measures variation of the RR interval.

Take 2 athletes, one with RHR of 47, one with RHR 48. One is over trained, the other isn’t. How do we differentiate between the two? Use HRV.

Fit athlete training well with adequate rest and recovery has HIGH HRV

Over trained, tired athlete not resting enough has a LOW HRV

Some HRMs have a “sleep test” function, which measures HR and RHR over a 4 hour window starting 30 minutes after you go to bed. From HR/HRV a Recovery Index is calculated which tells you whether your recovery is adequate. If you train a lot and are in danger of overtraining, a HRM

with a “sleep test” function will help you to balance training volume/intensity with adequate rest and recovery.

Druridge Bay Park Run 2.12.17

We had quite a day out at Druridge Bay last Saturday morning with several first time park runners from Physicality and Seahouses Striders taking part, along with the regulars.

Kath Douglas looking stylish and relaxed

Louise Dawson enjoying herself

Robert pacing Julie around the course

Carole heading for the finish line

Annette and Lesley working together at their first park run – a great achievement

Hopefully they’ll be many more park runs to come and with a personal time for the 5k, we all have a target to beat. Bring it on!

Food as Fuel for Athletes. What to eat and when to eat it Monthly Talk 4/12/17

Nutrition is crucial for athletic performance. Firstly, we need to eat optimally most of the time. But what we eat and when we eat it (before, during and after) with respect to workouts and races is key to getting the best out of yourself. Time and effort can be put into training over many months without paying enough attention to the fuel you need to maximise the return from that effort. Fuelling for workouts depends upon the volume, intensity and purpose of the workout. Races are different. And sadly, poor nutritional strategies can result in a disappointing race day. This talk discusses optimal nutrition for athletic performance and the principles of nutrition for a variety of workouts and races.

The basis of good nutrition is nutrient-dense food at every meal.

Colour is good!

And this “freedom food” turkey has had a good life and is full of nutritious protein






But before and after races or workouts our fuel needs special consideration and non-optimal foods (carbohydrates from grains and cereals) have an important role to play, along with protein rich in BCAAs (branch chain amino acids):

Here are the notes for the December talk covering this subject, with examples of fuelling strategies for different races or workouts.


Everyone wants to know what to eat and when with regard to optimising their performance in training, in post workout recovery and particularly in races. An unfortunate but common scenario is that people put in months of training building up to a particular race – then have a bad day. One reason for this can be poor nutritional preparation. Nutrition is ongoing and continual – it’s not just what you eat around a race or workout. But there are adjustments to be made to your food around a race or workout because FOOD is FUEL and your fuel requirements differ depending on the intensity and duration of the race or workout.

Here are some common examples of races and workouts for which your fuel needs consideration:

  •  steady 3 hour morning cycle ride
  •  5k or10k race
  • 1- 1.5 hour sprint duathlon
  • 2-3 hour standard triathlon
  • High intensity 40 minute interval session
  • Long slow training run
  • Strength and conditioning gym session
  • 1 hour personal training session

How does the requirement for and timing of fuel intake differ between these races/workouts?

To answer this question, let’s start with the two aspects of nutrition:

  1. What you eat
  2. When you eat it


 OPTIMAL FOODS –for health

Food should provide optimal nutrition i.e. we should eat what we have evolved to eat over the last 2.5 million years, which are the foods of the hunter-gatherer . These foods are high in nutritional value and are essential for growth, repair and maintenance of healthy tissues.

  • Lean meat
  • Poultry
  • Fish and seafood
  • Game meats
  • Vegetables
  • Fruits
  • Nuts
  • Seeds
  • Berries
  • Whole eggs

The more of these nutrient dense foods you eat, the better will be your health and athletic performance. They provide plenty of energy for all but high intensity or high volume training.

NON-OPTIMAL FOODS – for energy

Non-optimal foods are those of agriculture and dairy farming, which have been around for less than 10,000 years and which we have not evolved to eat. These foods mainly provide energy and are nutrient poor.

  • Grains e.g. oats/barley /rye
  • Wheat e.g. bread/cakes/biscuits
  • Cereals
  • Potatoes including sweet potato
  • rice
  • pasta

Whilst small quantities of these foods are not harmful, eating mainly these foods will diminish your health and vitality and reduce your fitness. They are an important source of energy for athletes.

  • Dairy products (milk, cream and cheese) are also non- optimal. They are nutritionally rich but many people cannot tolerate them and they can promote respiratory mucus so are avoided by professional cyclists.

So athletes who train at high intensity or for long periods regularly do need to eat these energy-dense non-optimal foods such as grains/wheat in the small windows of time before and after a workout to aid recovery and fuel performance.

For top performance, an athlete’s diet in the main should comprise optimal foods for health, with non-optimal carbohydrate rich foods just before or after a workout (see When to eat) for energy.


Industrially produced, processed and packaged foods

  • artificial fats (trans/hydrogenated/vegetable oils) and anything cooked in them
  • sugary foods such as chocolate bars/canned foods/soft drinks/”low fat” foods –  sugar promotes fat storage and hunger
  • ready meals and highly processed foods
  • junk/fast food
  • alcohol

 TREATS: A few suggestions might include:

  • Plain dark chocolate
  • Quality ice-cream made with milk/cream not vegetable fat
  • Stewed fruit with oat crumble
  • Flapjacks made with butter and some chopped dried apricots or dates or raisins/currants or nuts such as pecans to make them interesting and add some extra nutrients
  • Chocolate protein mousse made with coconut milk, cocoa powder, protein powder or eggs, honey– just whisk it all up and put in the fridge for an hour, fresh fruit on top


All the above foods are a combination of the 3 macronutrients, just in different proportions.


  • key for athletic performance
  • repairs damaged muscle, replaces red blood cells, maintains immunity
  • muscle protein is broken down during exercise and must be replaced
  • daily requirement for a 68kg athlete ranges from 84 to 168g protein per day (equivalent to 10-20oz of high quality protein such as steak, fish or chicken)
  • protein deficiency in athletes may cause frequent colds/slow recovery/irritability/poor response to training/chronic fatigue/sugar cravings
  • it is difficult to eat too much protein – any excess is converted to glycogen or fat and stored
  • provides 4kcals/gram


  • critical for fuel in endurance events, provide 4kcals/gram
  • Glycaemic Index: a ranking given to 50g of a carbohydrate food based on how quickly it causes blood glucose to rise compared to glucose (UK) or white bread (US), both of which have a GI of 100. Foods packaged by nature have a low glycaemic index (eg whole grains, oats, fruit, green vegetables) whereas processed foods have a high glycaemic index (eg refined cereals, white flour products, sweets, mashed potato, sugary drinks). Fat and protein reduce the GI as absorption is slowed. Mostly aim for low GI foods (LOW and SLOW) rise in blood glucose) except when you need a quick boost before or during exercise then choose a high GI food (HIGH and FAST)  such as a gel/glucose drink/energy bar.
  • Glycaemic load: a measure of the carbohydrate in one serving. Some foods have an apparently high GI but a low glycaemic load eg watermelon.
  • a high GI carbohydrate meal (e.g. cereal and toast for breakfast) causes an insulin spike which prevents the body from utilizing fat and when insulin falls a couple of hours later, creates hunger cravings
  • aim to eat carbohydrates which release glucose slowly i.e. “low  glycaemic index” foods such as apples, peaches, apricots and other fresh fruit, non-starchy vegetables
  • eat foods with a moderate glycaemic index  a couple of hours before and again after a workout (stages 3 and 4 – see later) i.e. wholewheat pasta, wholemeal bread, oats, potatoes, raisins and other dried fruit, cereals, rice, bagels, and some fresh fruits such as bananas, grapes, melon (combined with some protein)
  • combining fibre, protein or fat with carbohydrate slows glucose release (e.g. whole fruit not fruit juice, fruit with eggs) and lowers the glycaemic index
  •  a high carbohydrate diet reduces the use of fat as fuel for exercise, so limit carbohydrate foods  to post work-out refuelling
  • insulin-resistant athletes may be at risk of developing Type 2 diabetes if they continue to eat high carbohydrate diets for decades since such diets worsen insulin resistance
  • dietary carbohydrate restriction is the single most effective intervention for reducing all of the features of metabolic syndrome and should be the first approach in diabetes management, with benefits occurring even without weight loss


  • essential for good health (immunity, hormone production, skin and hair, nerve and brain cells, fat-soluble vitamins)
  • an efficient source of energy providing 9kcals/gram
  • eat  “good” fats i.e monounsaturated and omega-3 polyunsaturated fatty acids found in olives and nuts, oily fish such as salmon, tuna, sardines and mackerel, pasture fed animals i.e grass fed beef/lamb, free-range poultry, free- range eggs, butter from grass fed cows
  • use butter or animal fats (i.e. fats which are solid at room temperature) for pan-frying or high temperature cooking as liquid vegetable oils denature at high temperatures
  • AVOID saturated fats from cereal fed livestock, man-made trans and partially hydrogenated fats in cakes/biscuits/processed foods/margarines/fast food/junk food/fried foods/ready meals
  • Dietary calories can comprise up to 35% from good fats
  • Eating some good fats improves long term recovery and capacity to train at a high level and may improve racing performance if fat intake has been low
  • Long term adaptation to a high fat/low carbohydrate diet induces very high rates of fat oxidation during exercise – sufficient for most exercisers in most forms of exercise- without the need for added carbohydrate. Thus fat, including ketone bodies, appears to be the ideal fuel for most exercise – it is abundant, does not need replacement or supplementation during exercise and can fuel the forms of exercise in which most participate

A note about WATER

  • Drink water between workouts, not sports drinks or fruit juices. Don’t overdo it, aim for pale, straw-coloured urine
  • Add electrolytes to the water around workouts or use a sports drink
  • Use gels and water during a race OR sports drinks, not both
  • 68kg athlete needs 2 litres/day just for living (some supplied by food) plus replacement of fluid lost in training
  • 1kg body weight loss through exercise is equivalent to 1 litre water loss so you can work out how much you need to replace fluid lost in a workout – just weigh yourself before and after.


Protein and good fats are essential for health and athletic performance.

Carbohydrates are nutritionally poor but essential for fuel in endurance events and intake should be restricted to pre, during and post workout.


Eating at the correct time is essential for recovery. Time your carbohydrate intake around workouts.

This uses carbohydrate for fuel and recovery whilst reducing the total amount of carbohydrate in your diet and optimising nutrient dense food intake the rest of the time.

There are 5 stages for every workout:


  • Eat 200-300 calories per hour before eg 2 hours before the workout, eat 400-600 cals. If it’s 3 hours to the workout, eat 600-800 cals
  • Choose from moderate glycaemic index, carbohydrate rich foods to release energy slowly (pasta/whole wheat bread/rice/potatoes/oats/bananas etc)
  • Include some protein especially BCAAs ( branch chain amino acids – leucine, isoleucine and valine) which both lowers the glycaemic index of the carbs eaten at the same time and aids protein synthesis after the workout (eg boiled eggs and fruit, baby food, energy bar with protein)
  • For an early morning fat burning run/ride (NOT a swim), drink a sports drink OR a gel with some water 10 minutes before the workout. You won’t burn fat if you eat carbs for breakfast.
  • For a race, have a high glycaemic index food 10 minutes before eg gel/energy bar/handful of jelly babies or raisins. (Caffeine may be useful – to be discussed with supplements)

STAGE 2: DURING THE WORKOUT (up to 4 hours)

  • For an hour or less, drink water
  • For over an hour, drink a sports drink OR gels with an immediate large drink of water, not both
  • Sports drink should be 4:1 carb:protein mix with electrolytes (and possibly caffeine) in water, consume 2-300 cals/hour, small amounts every 20 minutes


  • The key time to take in carbohydrates as your body is several hundred times more sensitive to carbohydrates and will readily store more than at any other time – the carbohydrate window!
  • Use recovery drinks with about 2:1 carb:protein mix (higher protein than a sports drink) with electrolytes (make your own with fruit juice/protein powder/glucose powder/one fruit/pinch salt)
  • Consume 7-8 calories per kg body weight mostly from high GI carbohydrates (about 500 calories for a 67kg athlete) in the first 30 minutes post exercise, include protein,( BCAAs)


  • Continue to focus on carbohydrates plus some protein for a period of time equal to the length of the workout
  • Suitable foods are pasta/bread/rice/potatoes/sweet potatoes/oats/bananas/raisins plus some protein


  • Minimize starchy carbohydrate foods, avoid high GI foods altogether, they are low in nutrients, are quickly stored as fat and reduce your ability to metabolise fat when you exercise
  • Eat as much as you want of optimal foods i.e. lean meat, fish, fruit and vegetables
  • Protein is essential to rebuild muscle, many athletes don’t eat enough. The higher the intensity/volume of the race/workout, the more protein you need
  • Eat plenty of omega 3’s (essential polyunsaturated fats) from eggs/fatty fish/avocados/ nuts etc. They are ANTI-inflammatory and aid recovery, unlike omega 6’s from vegetable oils which are inflammatory
  • Snack on  fruit, nuts and seeds
  • Keep to small amounts of dairy
  • Be imaginative – have steak and vegetables for breakfast if you feel like it
  • AVOID processed food, especially “low fat” labelled foods as they are high in sugar and processed meats such as bacon, sausages, meat pies Be wary of food out of a factory, don’t eat it. If it is of animal origin and the animal has led a healthy life eating it’s natural diet in it’s natural environment, it is generally good to eat


What about the few days before a big race?

  • During race week, stick mainly to optimal foods
  • As race day gets closer, reduce fibre and increase carbs
  • Expect a weight gain of 2-3lbs – as you store glycogen in your muscles each gram of glycogen is accompanied by 2.6 grams of water – don’t worry about it, you’ll need both. An untrained person can store 400g glycogen in their muscles, a trained person twice that.
  • The day before the race, eat low fibre/high carb food with some fat and protein eg mashed potato/rice/fatty fish/chicken/steak/dried fruit. AVOID the pasta party the night before!
  • Drink water, not too much, add electrolytes in a hot climate or after a gentle pre-race workout

So now let’s go back to our original list of races/workouts and decide how to fuel for them (before, during and after). Water excluded.

  • steady 3 hour morning cycle ride
  •  5k or10k race
  • 1 hour sprint duathlon
  • 2 hour standard triathlon
  • High intensity 40 minute interval session
  • Long slow training run
  • Strength and conditioning gym session
  • 1 hour personal training session
STEADY 3 HOUR MORNING CYCLE RIDE Small portion carbohydrate eg banana/energy bar Few dates/handful nuts and raisins/banana Carbohydrate snack within 30 minutes, carb/protein meal  within 1-2 hours
5K or 10K RACE 2—300cals carbs/protein 2 hours before, gel or high glycaemic carb snack 10 minutes before Nothing Carbohydrate snack or recovery drink immediately you finish

Carb/protein meal  within an hour

1 HOUR SPRINT DUATHLON As for 5/10K race Nothing OR gel after 30-40 minutes plus water OR  sports drink As for 5/10K race
2 HOUR STANDARD TRIATHLON 4-600 cals carb/protein 3 hours before OR 6-800 cals 4 hours before

Low fibre high carb snack 1-2  hours before eg

toast and jam/banana and honey in a little porridge/rice pudding

Gel/energy bar 10 minutes before race

Gel plus water OR sports drink every 20 minutes from 30 minutes into race Recovery drink immediately

Carb/protein snack as soon as you can face one

Large carb/protein meal  within 2 hours

HIGH INTENSITY 40 MINUTES SESSION If it’s first thing in the morning, light breakfast eg protein pancakes with fruit/ eggs and fruit/veggie omelette/ coffee with energy bar

If during the day, carb/protein snack 1 hour before OR nothing BUT don’t start hungry

Nothing Recovery drink immediately

Carb/high protein meal within 1 hour

LONG SLOW TRAINING RUN If early morning, small portion carbohydrate eg banana/energy bar

Otherwise, nothing, just don’t start the run hungry

Nothing Carbohydrate snack within 30 minutes then carb/protein meal within 1-2 hours
STRENGTH AND CONDITIONING GYM SESSION Carb/protein snack 1 hour before eg eggs and fruit Nothing Carb/high protein snack/recovery drink  immediately you finish Carb/high protein meal within 1 hour
1 HOUR PERSONAL TRAINING SESSION If early morning, banana/energy bar/few dates and nuts

If later, nothing BUT don’t start hungry

Nothing Carb/protein snack /recovery drink immediately you finish

Carb/high protein meal within 1 hour

Detailed example fuelling strategy for a standard distance triathlon as given to me by Lisa Williams (Physicality client and experienced GB age group triathlete):

“My usual fuelling strategy for standard distance would be to increase carbs and ensure I’m well hydrated in the 2-3 days before the race.

 The evening before race day I would include either rice or potatoes in my meal choice and usually stick to chicken as a protein source. I would again make sure I’m well hydrated and use SIS electrolytes in my water.

 Race morning I would drink electrolytes up until 1 hour before race start. Breakfast 3 hours before is normally porridge and a coffee. I would eat a banana 1-2 hours before race start to top up my carb stores.

 Once on the bike I would have a gel usually at 1hour through the race, then a gel at 1hr 30, 10mins before I’m due to finish the bike I would take a caffeine gel to prepare for the run.

 On the run I take a gel after 30mins and have a 2nd gel in reserve in case I’m flagging.

 Ideally post race I’d take in a liquid recovery drink e.g. SIS recovery (easily mixed with water and portable) within 15mins of finishing. I can rarely stomach solid foods straight after racing but aim to have a good protein and carb rich meal within 2-3 hours. Something like steak and chips or whatever I feel like eating once my appetite returns. I always try and rehydrate also”.



The Cyclists Training Bible (Joe Friel  2009) Chapter 16

The Paleo Diet for Athletes  (Loren Cordain and Joe Friel)

Nutrition and Physical Degeneration (Dr Weston Price)

“It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet”            BJSM 23/4/15 Malhotra, Noakes and Phinney


Physiology of Exercise 1 – Aerobic capacity monthly talk 6/11/17

Aerobic capacity is the ability to take in, transport and utilize oxygen and is a major factor in endurance performance. So when we train,  increasing our aerobic capacity is always a goal.

But how does this happen? How does the body handle oxygen?  How do we measure aerobic capacity and what are the physiological effects of training on the way we handle oxygen?

Here are the notes from the talk which attempted to address a massive subject and summarise the main points.



WHAT (physiological parameters) are we training and why, not HOW to train them. That comes later!

Aerobic Capacity is the ability to consume O2.

(See pdf file Doc_752043 also at the foot of the page for supporting diagrams Figure 2 – Carl’s blood lactate curve.)

Endurance athletes have superior aerobic energy transfer and so aerobic capacity is a major factor in endurance performance.

Maximum O2 consumption is referred to as VO2max.(See Figure 3 – VO2max/lactate/running speed treadmill test)

It represents the maximum amount of O2 that can be removed from the circulating blood and used by the working muscles. Elite athletes have around twice the VO2max of sedentary people. A high VO2max requires integration of pulmonary, cardiovascular and neural systems and is a good indicator of endurance performance.

However, VO2max is NOT the sole determinant of endurance performance. Other factors, mainly at the local tissue level strongly influence a muscle’s ability to utilize oxygen and hence the ability to sustain a high level of aerobic activity.


Absolute VO2max is measured in L/min. Relative VO2max is measured in ml/kg/min and takes in to account the body mass of the subject. For example:

-a huge rower 120kgs may have an absolute VO2max of 7L/min which is a relative VO2max of 7000/120=58mls/kg/min.

-a petite cyclist 50kgs may have an absolute VO2max of 4L/min which is a relative VO2 max of


So the cyclist can consume more O2 for their size.

Average relative VO2max for 35yo men in the general population is around 35mls/kg/min.

It declines with age and is lower for women.

Table of relative VO2 max scores for elite sports (mls/kg/min)

>75 Elite runners, cross country skiers, cyclists
65 Squash players
60-65 Premiership football players
55 Rugby
50 Volleyball
50 Baseball


VO2 max is a good indicator of endurance performance. It will differ between sports in the same person as the exercise requirements are not the same eg running involves more all body activity than cycling, so running VO2max will be higher .

For interest

Carl:   Cycling VO2max = 68mls/kg/min                Carole:  Cycling VO2max 58 mls/kg/min

Running VO2max= 77mls/kg/min

What are the physiological steps in the consumption of oxygen? See Figure 1

  1. Ventilation – LUNGS
  2. Circulation –CARDIOVASCULAR SYSTEM (heart, blood vessels, blood)
  3. Oxygen utilisation – MUSCLES


O2 =21% of inspired air

Airways – mouth/nose/trachea/lungs/bronchi/bronchioles/alveoli

Chest cavity (thorax) – negative pressure from diaphragm contraction/other respiratory muscles causes inspiration, relaxation of diaphragm – expiration (passive at rest). Rises in CO2/H+  levels are the stimulus to breathe, not lack of O2.

FVC = Functional Vital Capacity = max inspiration – max expiration over 1 second

FVC is 4-5L in men and 3-4L in women, is mainly genetic and is NOT altered by training

FVC is NO indication of aerobic fitness or performance as long as it is within a normal range and untrained people the same size as a trained athlete may have similar FVCs.

Alveolar gaseous exchange – diffusion of O2 to the red blood cells (rbcs) and return of CO2

Gaseous exchange is NOT a limiting factor in O2 uptake except in disease

Blood flow velocity is NOT a limiting factor either (except in EIH=Exercise Induced Hypoxia in elite athletes, thought to be a ventilation/perfusion mismatch)

Women have smaller lungs, reduced lung function measures, reduced airway diameter and reduced alveolar surface area even after allowing for their smaller stature and so have reduced aerobic capacity than men.

Exercise Hyperpnoea = desperate gasping/heavy breathing at intense levels of exercise is NOT due to inability to breathe in enough O2 as alveolar O2 levels rise and CO2 levels fall in this state of hyperventilation. Stimulus for this is thought to be neural.


  • Pulmonary ventilation does NOT limit maximal aerobic performance (normal FVC, no disease)
  • Larger FVCs are genetic
  • Untrained individuals are breathless due to a failure to regulate blood CO2/H+ levels
  • Exercise Hyperpnoea (hyperventilation) at intense levels is NOT due to lack of O2
  • Women have lower ventilatory capacity than men
  1. CIRCULATION – CARDIOVASCULAR SYSTEM (heart, blood vessels, blood)
  • Heart – a pump, 4 chambers, receives deoxygenated blood from the organs and muscles, pumps it to the lungs from which oxygenated blood returns to be pumped back out to the organs and muscles again
  • Arteries –  a high pressure delivery system, muscular walls, pulse, systolic and diastolic pressure
  • Capillaries – exchange of gases, very small, dense network, site of gaseous exchange
  • Veins – low pressure return system, thin walled, no muscles, rely on muscle pump (death by crucifixion/post race collapse), flow direction controlled by valves
  • Blood – cells suspended in plasma. Red blood cells carry O2 from the lungs to the muscles by binding it with haemoglobin Hb

Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)

What happens to the CV system on exercise?

Stroke Volume SV

SV is higher at rest to start with in trained athletes.

On exercise SV increases with intensity  up to an exercise intensity of about 50%VO2max then plateaus. Further increases in CO are due to an increase in HR only, until max HR (and max CO) is reached.

Heart rate HR

Increases with intensity rapidly within 30 seconds to 2 minutes of a run then gradually increases further to a maximum, roughly (10% variation) 220-age

Why is HR lower in fit people? SV increases with training.

At rest, 75kg male has a CO of 5L/min.

Untrained:  HR is ~70bpm, SV = 5000ml/70 = 71mls

Trained:      HR is 50bpm,   SV= 5000ml/50 = 100mls

Cardiac Output CO

College students increase their CO 4x to 20L/min on maximum exertion (max HR 195)

Elite athletes increase their CO 7-8x to 35-40L/min (SV = 180-200mls) (max HR 195)

Racehorse max CO = 600L/min!

The changes in SV (and hence CO) are due to increases in:

  • Blood volume (increased plasma volume – increased “preload”)
  • Mycocardial (heart muscle) contractility (Frank-Starling mechanism i.e. force of contraction is proportional to the initial length of the muscle fibre))
  • Compliance (elasticity) of the left ventricle

and are a result of training.

Larger SV ~ larger CO ~larger VO2max ~ enhanced endurance performance

Myocardium (heart muscle)

Relies on aerobic metabolism and has 3x the oxidative capacity of skeletal muscle.

At low exercise intensities it oxidises mainly fat. At moderate intensities it oxidises both fat and glycogen. Trained heart muscles uses more fat and spares glycogen, as does skeletal muscle.At high exercise intensities it oxidises lactate as fuel (produced anaerobically by the skeletal muscle).

Blood Pressure

Normal BP 120/80mmHg, high >140/90, low 90/60 or less

Systolic BP increases rapidly with exercise at first then in proportion to intensity, reaches about 200mmHg. Increase in mean arterial pressure combined with reduced peripheral resistance as blood vessels dilate (resistance to flow is inversely proportional to radius to the power of 4 (eg if the radius doubles the resistance to flow falls by a factor of 16, so a small dilation massively reduces resistance to blood flow)

Diastolic BP remains stable or falls slightly due to blood vessel dilation.

Blood (= rbcs suspended in plasma)

  • Rbcs

Rbcs carry O2 from the lungs to the working muscles,bound to Hb

At the muscle cell, myoglobin Mb has a greater affinity (250x) for O2 than Hb and so the O2 moves from the rbc to the muscle cell. CO2 moves out from the muscle cell to the blood and is carried away  dissolved in plasma (as H+ and HCO3-) to the lungs where it is breathed out (as CO2 and H2O).

Number of rbcs (haematocrit) increases with training. Normal range is 39-50% (men) 35-44% (women).

Concentration of Hb in rbcs increases with training.

Dietary Fe important – main sources of haem iron are red meat, fish seafood, poultry and other animal products, also in leafy green veg. Non haem iron is found in plants and is more difficult to absorb, hindered by phytates in some vegetables and pulses and by dairy products.

Iron deficient anaemia is common in female endurance athletes, reducing their aerobic capacity.

Women have 5-10% less Hb per L than men.

Rbc production is stimulated by lack of oxygen ( hypoxia) in the working muscles, causing release of Hypoxic Factor which stimulates release of EPO (erythropoietin) from kidneys which stimulates bone marrow to produce more rbcs.

Note – training must be of sufficient intensity ( i.e.around LT) for adequate time and repeated bouts of training for Hypoxic Factor to be released.

Blood doping – autologous blood transfusions or injecting with EPO, dangerous increases in blood viscosity result.

  • Plasma

Plasma volume increases with training.

Untrained haematocrit 45%, plasma 55%

Trained haematocrit 38%, plasma 62%

So a trained athlete is borderline anaemic on standard blood tests with a haematocrit of 38% (normal range 38-50% for men), due to increased plasma volume. However, total rbc mass increases as well. The increased blood volume increases both SV and total rbc mass, thus increasing CO and aerobic capacity.

Capillary network

Only one cell thick wall (i.e. very thin), rolled up, with a diameter of 1/100th mm=one rbc wide. At rest only 1/40th of the capillaries are open.

Muscle and heart capillaries dilate massively on exercise to increase the blood flow and O2 supply (reduced “afterload”).

Controlled by autonomic nervous system (sympathetic/parasympathetic). HR and blood flow to muscles increase in anticipation of exercise as a result of training the neuromuscular pathways (148bpm before 100m sprint, 122bpm before 800m, 118bpm before 1m, 108bpm before 2m races)

“Shunting” of blood away from non-vital organs and the skin (5% blood to skin at rest, 20% during exercise in warm conditions but shunting away from the skin still occurs on maximal exercise).

Cardiac drift

In prolonged periods (>15 minutes) of submaximal exercise, SV falls and HR rises as intensity remains constant. Due to sweating and an increase in core body temperature causing a fluid shift from the plasma to the tissues, so plasma volume falls and SV falls, reducing VO2max. A trained person has reduced cardiac drift.


Finally the oxygen laden blood arrives at the muscles. O2 uptake and utilisation at the muscle depends upon the following factors:

Density of the capillary bed – a network of tiny blood vessels throughout the muscle.

Blood flow

Muscle myoglobin concentration (Hb4O8 releases O2 to 4MbO2)

Oxygen exchange rate

Size of mitochondria

Number of mitochondria

Oxidative enzymes

Aerobic ATP production in mitochondria

ALL of these increase with training, thus increasing aerobic capacity.


Important factors which influence endurance performance are:

  1. Aerobic capacity – the ability to consume oxygen
  2. VO2max – maximum capacity to consume oxygen
  3. Lactate Threshold – maximum level for steady state exercise

The main variables affecting aerobic capacity, VO2max and LT are:

  • CO (cardiac output) , which depends on heart rate and stroke volume
  • Haemoglobin concentration
  • Erythrocyte (red blood cell) production
  • Capillary density in the muscles
  • Oxidative enzymes in the mitochondria of muscle cells
  • Running economy

Take home message:

Endurance training at different levels of intensity enhances aerobic capacity.

Training must include intensities at or around LT, for an adequate length of time per workout and workouts at this level must be repeated.

VO2max may not increase following training whilst endurance performance does improve.

As endurance is performed at LT (race pace) not at VO2max (a higher level of intensity than LT), training induced improvements in performance correlate more with training an increase in LT than with changes in VO2max.

LT increases with training due to improved aerobic capacity at lower intensity of exercise

(see figure 4 – Effect of training on LT).

Think of it a bit like HR. Training doesn’t change your max HR, but resting HR is lower if you are fit because you are physiologically more efficient. Similarly training doesn’t necessarily increase your VO2max, but your ability to consume oxygen (aerobic capacity) at submaximal exercise intensities (up to LT) does. Your LT increases, as you can utilize oxygen better and delay going anaerobic.

So you can run faster at your race pace (LT).

The diagrams to support this text can be found below:





  1. The Science of Running Steve Magness 2014
  2. Exercise Physiology – Nutrition, Energy and Human Performance MacArdle, Katch and Katch 8th edition 2015
  3. Daniels Running Formula  Jack Daniels PhD 3rd edition 2014
  4. The Cyclist’s Training Bible Joe Friel 4th edition 2009
  5. Triathlon Science Joe Friel Jim Vance 2013

Nutrition and Physical Degeneration – monthly talk 9/10/17

For those of you who were unable to attend the talk, here are the notes:



Here’s an excerpt from the Financial Times Weekend dated 16/7/17. A panel of experts were asked “What’s the big, bad idea?” within their field of expertise. This is the answer given by Stephen Westaby, a heart surgeon:

“One of the most interesting pieces of news to come out of the (recent conference of the) European Society of Cardiology was that people who have a low-fat diet have a higher mortality rate. For years and years and years, we’ve been flogged with advice to avoid bacon, to avoid eggs, to avoid cheese. A very large study has shown that those who take a low-fat diet have about a 25% chance of dying earlier, either from heart disease or cancer. So we’ve had 25 years of misinformation”.

Study: 135,000 people in 18 countries:

  • Low intakes of saturated fat increase chances of early death by 13%.
  • Consuming high levels of all fats cuts early death rates by up to 23%.
  • Carbohydrate-laden diets are amongst the most unhealthy with those eating refined sugar and processed meals having a 28% higher risk of early death.
  • Getting 35% of calories from fat was the “sweet spot”.

So what has happened to our diet and health? How come we’ve had “25 years of misinformation” which has increased our risk of heart disease and cancer? On what evidence exactly was this “misinformation” based? How has our diet actually changed over the years and why did those changes occur in the first place? Are all of the “Western diseases” of tooth decay, obesity, heart disease, high blood pressure, type 2 diabetes, bowel disease, NAFLD, stroke, cancer and Alzheimer’s associated with a “Western” diet and has their incidence increased with changes in diet?

In order to answer these questions, we must take a logical approach and look at the following:

  1. The human diet through the ages to see what foods we evolved to eat
  2. The incidence of “Western” diseases in populations eating traditional foods
    rather than a Western diet
  3. How “civilisation”, industrialisation and political intervention based on bad science
    has altered our diet
  4. How the incidence of disease has changed with diet.

The simplest approach is a chronological one. So we are going to start by looking back not just 25 years, but two and a half million years.

Nutritional Timeline

2.5 million years ago to about 15,000BC-Paleolithic era. Marked by the use of stone tools by early Homo habilis who evolved into Homo sapiens during this period. Hunter-gatherer diet, wide variation of plant/animal sources.

 Agricultural revolution  10,000 years ago, early growing of wild cereals mainly in the East, domestication of animals and settled populations

Industrial revolution 200 years ago in 1800s and importation of sugar from Caribbean/slave trade, mechanisation of food production. Appearance of diabetes (rare, 1-2 per 1000) and obesity only amongst the affluent. Sugar consumption per person per annum was about 5lbs.

Early 1900s- 2nd WW– trans fats and processed foods, steady level of sugar consumption, less during WWs. Diet low in refined carbohydrates was the standard treatment for obesity across Europe. Grandparents knew to avoid starchy food or get fat. Sugar consumption was about 40lbs pp pa.

1930s- Nutrition and Physical Degeneration by Weston Price, a masterpiece of nutritional science. One man’s study of the effects of a “Western” diet on hunter-gatherer populations – “Western” diseases previously absent appeared within a generation. The photographic evidence of the physical degeneration resulting from the abrupt change from indigenous foods to a Western diet is painstakingly recorded in a multitude of “primitive” populations across the world.

Observing healthy, remote populations untouched by the West, he found perfect dental arches, minimal tooth decay, high immunity to tuberculosis and infectious diseases and absence of “Western” diseases. On introduction to modern foods, white flour, white sugar, refined vegetable oils and canned goods, signs of physical degeneration quickly followed. Dental caries, deformed jaws, crooked teeth, club feet, increase in “mental defectives” and a low immunity to tuberculosis and other infectious diseases became rampant.

1950-1970s– an “epidemic” of heart disease (CHD). Loss of European scientific papers (especially those in German) expressing the view that obesity was due to refined carbohydrates and sugar. Sugar consumption was about 70lbs pp pa.

1970s– Big debate on the dietary cause of CHD – fat or sugar. Sugar consumption now about 100lbs pp pa (ie we were eating in 2 weeks the sugar our ancestors of 200 years ago ate in a year). Ancel Keys (cholesterol/saturated fat) vs John Yudkin (sugar). Seven Countries study (trans fats included in studies at this time, also not yet known that there are 2 types of LDL and TGLs difficult to measure). French paradox.  Food industry supported Keys, his laboratory financed by US Sugar Association; Prof. Yudkin personally and professionally attacked by British Sugar Foundation, wrote “Pure, White and Deadly”.

1977 – a defining moment George McGovern, Chairman of US Committee on Nutrition, a politician, decided it was fat causing CHD, against scientific advice that the fat/CHD hypothesis was unproven and the effects of a low fat diet were untested and unknown. His decision led to “Dietary Goals for the US” in 1980, the start of the low fat/high carbohydrate diet. Advice was to reduce dietary fats (from 40% of dietary calories to 30% with no more than one third from saturated fat) and increase carbohydrates (to 55-60% of dietary calories).

1992 US Food Pyramid. The first chart suggested to the USDA by nutritional experts in 1980 featured fruits and vegetables as the biggest group, not bread and other starchy foods. The original research based ‘Pyramid’ emphasized eating

  • more vegetables and fruits, with this group at the base of the pyramid
  • less meat, salt, sugary foods, bad fat, and additive-rich factory foods.

This chart was overturned at the hand of special interests in the grain, meat, and dairy industries, all of which are heavily subsidized by the USDA. If Americans followed the chart suggested, they would buy much less meat, milk, and bread. However, the original composer of the food Pyramid, Luise Light warned that if they ate as the revised chart suggested, it “could lead to an epidemic of obesity and diabetes

USDA censored that research-based version of the food guide and altered it to include more refined grains with 6-11 portions of bread, cereal, rice and pasta, only releasing their revamped version in 1992, 12 years after it was originally scheduled for release.

2005 US Food Pyramid.  The new 2005 Pyramid was again criticized as being heavily influenced by the food and drug industries. A series of research articles in 2013 and 2015 demonstrated that the dietary data used to develop the US Dietary Guidelines were “incompatible with survival” and should not be used for public policy.

A research paper in the British Medical Journal in 2016 states that the scientific committee advising the US government has not used standard methods for most of its analyses. It instead relies on the American Heart Association and the American College of Cardiology which are heavily supported by food and drug companies.

UK advice followed that of the US over this period. NHS advice is currently in the form of the Public Health England “Eatwell Guide” (2016).

1977-1996 low fat / high carbohydrate diet advice changes the food industry products and the dietary patterns of the population  As government advised us to eat a low fat/high carbohydrate diet, the food industry responded by making foods predominantly low fat/low cholesterol, increasing the use of manufactured fats and sugar. Consumption of butter fell by 38%, meat by 13% and eggs by 18%, whilst grains/sugar consumption soared by 45%. Obesity rates and diabetes soared too, as predicted back in 1980 by Luise Light in his objections to the 1992 US Food Pyramid, revised by the USDA under pressure from the food industries.

Present Day 2017 – Sugar consumption now about 150lbs pp pa – over 20 times that of 200 years ago. In 1975, 105M people obese globally. In 2014, the figure was over 6 times higher at 641M. Currently in the UK, over two-thirds of people in the UK have a BMI over 25 and are either overweight or obese. By 2025, 38% are expected to have a BMI over 30 and be obese. Type 2 diabetes affects 9% (about 3.5M) in the UK with a further rise to nearly 5M predicted by 2035. Obesity and diabetes are associated with higher risks of kidney disease, CHD, and vascular disease such as strokes. Yet Type 2 diabetes is “largely preventable” according to the director of the NHS Diabetes Prevention Program.
US Obesity levels have soared from 10-15% in the mid 1970s to nearly 40% in 2017.

Annual per capita sugar consumption has increased from 5lbs per person in the 1800s to 150lbs today.


History shows us that populations eating a hunter-gatherer diet of meat, fish, fruit, vegetables, eggs, nuts, & seeds, which is low in processed foods, sugar, refined carbohydrates and manufactured fats, do not suffer from Western diseases. Even today, the Masai subsist on cattle blood, meat, milk and little else. Native Americans subsist on beans and maize. And the Inuit in Greenland subsist on whale blubber and a bit of lichen. These populations are unaffected by Western diseases.  In the 1930s, Weston Price showed us that the introduction to a hunter-gatherer population of a “Western” diet, i.e. a diet high in refined carbohydrates, flour, processed fats & sugar, is associated with the appearance of physical degeneration within just one generation.

Yet despite this nutritional knowledge, the “Western” low fat high carbohydrate diet has been US and UK government advice for decades and remains government advice today. The irony is, the one diet we have invented for ourselves – the Western diet – is the one that makes us sick. As the cardiologist Stephen Westaby has just said, we have had “25 years of misinformation”.

(Note: I am assuming that “25 years” is referring to the first US Food Pyramid published in 1992.)

The result?  Physical degeneration. We now have unprecedented levels of obesity and diabetes (with the possibility that other Western diseases hypertension, heart disease, Alzheimer’s, NAFLD, bowel disease and cancer share a common cause – to be discussed another time).

Current evidence clearly shows that the low fat/high carbohydrate diet is unhealthy. Low saturated fat intake increases your chance of early death whilst higher fat intakes reduce it, and high carbohydrate diets have the highest risk of early death. The emphasis on calories, “eat less, move more” is based on the flawed energy balance equation (again the subject of a future talk!). The food industry declares that calories from sugar are fine as part of a “calorie controlled diet” rather than examine the effect of sugar on our health. Government blames the individual for poor dietary choices contributing to their health problems rather than question their own dietary advice.

Comments on diet by eminent physicians 200 years ago show that the cause of obesity (starchy, sugary foods) was already recognised:

“Taken in tea, milk and beer, sugar has caused lean people to grow fat” Benjamin Moseley (1799)

Weight gain is due to eating too many “fattening carbohydrates” and “many of our diseases may be attributed to too free a use of sweet food” William Banting, Letter on Corpulence (1863)

“Sure enough, carnivorous animals never grow fat (consider wolves, jackals, birds of prey, crows, etc.). Herbivorous animals do not grow fat easily, at least until age has reduced them to a state of inactivity; but they fatten very quickly as soon as they begin to be fed on potatoes, grain, or any kind of flour. … The second of the chief causes of obesity is the floury and starchy substances which man makes the prime ingredients of his daily nourishment. As we have said already, all animals that live on farinaceous food grow fat willy-nilly; and man is no exception to the universal law”. Brillat-Savarin, Jean Anthelme (1825). The Physiology of Taste.

So, what does history tell us to eat?

Populations which eat indigenous food are healthy. Introduction of processed foods, white flour, sugar and processed fats coincides with physical degeneration. Government advice since 1980 has been to increase our consumption of these modern foodstuffs. Our health has worsened. Ironically, despite the affluence of the West we suffer physical degeneration due to malnutrition. What to do?

Stop and think. Look at what is in front of you. Is it really food?

Nutrition author and harsh critic of US food policies Michael Pollan coined the phrase “foodlike substances”-  stuff to be avoided (i.e. processed foods, anything out of a factory, anything with a long list of ingredients, anything with ingredients you can’t pronounce, anything which doesn’t eventually rot, anything your great grandmother wouldn’t recognise as food). “Food” means real food – vegetables, fruits, meat, fish, seafood, eggs, whole grains, nuts, seeds, dairy). His dietary advice (7 words) is simple:

“Eat food, not too much, mostly plants”.

And we’ll leave the last word with Marie Antoinette:

“There is nothing new, except what has been forgotten”

Reading List:

  1. http://www.nhs.uk/Livewell/Goodfood/Pages/the-eatwell-guide.aspx
  2. “The Obesity Code” (2016) by Dr Jason Fung
  3. “Nutrition and Physical Degeneration” (1939) by Weston A Price DDS  with many reprints
  4. “Pure, White and Deadly: The Problem of Sugar” (1972) by Professor John Yudkin
  1. “The Paleo Diet” (2011) by Dr Loren Cordain
  1. “The Paleo Diet for Athletes”  (2012) by Dr Loren Cordain and Joe Friel
  2. “The Case Against Sugar” (2017) by Gary Taubes
  3. “Fat Chance: The Hidden Truth About Sugar, Obesity and Disease” (2014) by Dr Robert Lustig
  4. “Human Evolution, Diet and Health-The Case for Paleolithic Nutrition” (2008) Mark Hines
  5. “It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet” by Malhotra/Noakes/Phinney British Journal of Sports Medicine 23/4/2015
  6. “The Great Cholesterol Myth” (2012) Bowden/Sinatra
  7. “The Primal Blueprint” by Mark Sisson (2012)
  8. “Why We Get Fat and What To Do About It” by Gary Taubes (2012)
  9. “The Great Cholesterol Con” by Dr Malcolm Kendrick (2008)
  10. “Western Diseases: Their Emergence and Prevention” Hugh Trowell and Denis Burkitt (1981)
  11. “Rebuilding the Food Pyramid” by WC Willett and MJ Stampfer (Harvard School of Public Health) Scientific American 288 no 1 (Jan 2003) 64-71
  12. https://www.theverge.com/2015/2/9/8003971/low-fat-dietary-health-goals-bad-science






NB:The above aims to inform so that individuals can make their own dietary choices – it does not constitute dietary advice.