Why you are designed to eat and burn fat…your big brain

photo

I’ve just finished a couple of public lectures and had a big two page spread and a front page piece in the national newspaper about our work in low carb high fat eating. That’s prompted quite a few questions about how some people can eat carbs and not get sick.  

Here are a few of these questions:

“Why are some people and populations fine on higher carb diets?”  

“Why are you promoting a higher fat lower carb approach given many people (and sometimes populations) exist disease free eating higher carb diets?”

“Why do I put on weight so easily and others don’t?” 

“How does a low carb approach change things?”

These questions are very important and I think understanding the answers helps us understand the whole situation. My take is simplified into this:

Insulin is a hormone produced by the pancreas which helps move glucose into cells. It is essential for life.

Sometimes cells become resistant to insulin so it is harder to move the glucose onto those cells. This, no surprise, is called insulin resistance.  Insulin resistance is a normal and useful human condition, at least in our natural (ancestral) environment.

Humans very easily develop insulin resistance for two historical (and evolutionary useful) reasons.  First , in times of starvation, insulin resistance helps shunt any extra glucose to the large, energy demanding brain (12-1400 cc and consuming around 25% of our energy). This temporary peripheral insulin resistance helps turn on fat burning and when extra carbs are eaten, there is very little insulin response because glucose can be taken up in the brain without insulin.
The second reason to develop insulin resistance is to store fat in times of plenty of food. This system is mostly stimulated by high carbohydrate foods. The resulting chronic high insulin response shuts off fat burning, down regulates spontaneous energy expenditure, blocks leptin, and stores extra energy as fat. This metabolic syndrome probably works best as a temporary and seasonal effect.  I think we see this in animals preparing for hibernation who need to store fat as they subsequently rely on it as a fuel source for extended periods. The idea is that we can’t down regulate brain fuel demands, so need fat stores to help with this. We have much more fat mass and less lean muscle mass than a chimp who has a brain 1/3 the size of ours. So really the evidence is that we are designed to store and use fat. We easily put weight on to provide a source of constant fuel through fat for times of low food availability.
So insulin resistance is a really useful mechanism in human evolution and survival.  The problem now though is that insulin resistance is also caused by inflammatory processes and other means through the following things at least (there are probably more) – stress, poor sleep, too much exercise, too little exercise, high sugar diet, high Omega 6/trans fat diet, poor gut micro biome, high alcohol diet, age?, obesity, genes, smoking, pollution, other environmental toxins, too much sun, too little sun……
So I think you see the problem.  Modern life induces insulin resistance.  Some are more prone than others.
When you become insulin resistant then you will have trouble moving carbs (glucose) into your cells.  You probably will be able to do this, but just need loads of insulin to do so. So a relatively high amount of even “healthy carbs” for the insulin resistant person can result in constantly high insulin. We call this “hyperinsulinemia”.
This condition is probably the mechanism which causes most modern chronic diseases – cancer, diabetes, CVD, and neurological degeneration. Hyperinsulinemia is the direct and indirect cause of these. The mechanistic, epidemiological, and experimental evidence is strong.
Chronic hyperinsulinemia probably also makes you more insulin resistant and it becomes a vicious cycle.
Here’s why:
  • Humans who are not insulin resistant can thrive on higher carb diets as long as they don’t live a western industrial food and stress lifestyle.
  • Modern society is toxic in so many ways to our basic function – because it induces insulin resistance through inflammation.
  • Reducing dietary carbs for those who are insulin resistant (also know as metabolically dysregulated, also sometimes called carbohydrate (in)tolerance) is a useful way to proceed. Probably we can reset the system using this method, but we must first stop chronic hyperinsulinemia. More work needs to be done to understand exactly how this might work and if and when carbs might be eaten again in bigger quantities.
  • Living a life which resembles that of your ancestors minimises our chance of becoming metabolically dysregulated.
  • People vary in their personal carbohydrate tolerance and how that affects their health because they vary in their insulin resistance.
  • When you go on a low carb high fat diet you can burn fat, feel energised and easily manage your own hunger and eating.  Will power is over rated, especially in the face of dysfunctional physiology.
Anyway that’s a quick scientific primer from my perspective and the basic mechanisms behind what I am talking about. Here’s a reference for the adventurous and scientifically minded which goes in to more detail – Lifestyle and nutritional imbalances associated with Western diseases: causes and consequences of chronic systemic low-grade inflammation in an evolutionary context
 

Why dogs are good for you

photo[3]

I’ve had three family dogs – all border collies. The one in the picture is Bluey, a 15 month old red/white border collie. He’s a friendly and active fellow, on a whole food meat and other stuff based diet.

I wanted the smartest, most active dog because my view was that they would need exercise and that would force me and the family to do more exercise.  So is that likely to work, or is the dog more trouble than he’s worth and you just spend more money and can’t holiday when and where you like?

Well the original big dog in the research into dogs and physical activity was Prof Adrian Bauman and his dog Schroeder (a Jack Russell). Schroeder is the first dog I know to be a published author on a research paper.

Anyway, Adrian is back with a team reviewing the benefits of dog ownership on physical activity in the latest issue of the Journal of Physical Activity and Health.

There are now 29 studies looking at this, including one by me almost 10 years ago.  I showed that dog ownership wasn’t enough; you needed to have at least a middle to big sized dog!

So what has the latest review shown? “Approximately 60% of dog owners walked their dog, with a median duration and frequency of 160 minutes/week and 4 walks/week.” Dog owners on average are slightly more active than non-dog owners, but the effects are small. We don’t know if giving someone a dog helps them be more active. In other words, we need dog intervention research!

So is it worth having a dog?  Probably. There are numerous benefits, including some extra activity. Are there hassles? Damn straight there are.  Mine crapped in the kitchen overnight and I was the one who got in trouble for it, and I even cleaned it up!

There’s something else about being out with a dog too.  The sheer primal nature of it, the ability of the dog to draw you into the moment of being alive.  Running on an empty beach.  Chasing seagulls.  It’s great fun.

photo[2]

What if I ate less?

photo[1]

What would happen if I ate less?  Here’s a theoretical question from a reader.  I’ve been mulling it over as it is really fundamental to what I am talking about. Here’s the question:

Professor Schofield, I have a situation for you and I would love to hear how you respond.

Given three identical 100-kg individuals (assume they are a model of a human that experiences no natural desires or whims to suppress or appease) who all burn kilocalories at a rate of exactly 2500 per day. Assigning letters ‘A’, ‘B’ and ‘C’ to these individuals.
‘A’ consumes exactly 2000-kcal per day eating nothing but candy.
‘B’ consumes exactly 2000-kcal per day eating nothing but vegetables.
‘C’ consumes exactly 2000-kcal per day eating nothing but meats.
How are the bodies of ‘A’, ‘B’, and ‘C’ going to change in 60-days?

I have read many of the points made on this blog that a calorie is not a calorie and I also understand that all three of the above diets are pretty unrealistic; however, my math background wants to align myself with the law of the conservation of energy and say that they would all lose approximately the same amount of weight.

Your response is appreciated.

OK here’s what I think would happen, and there is some evidence around this, although as usual, more metabolic wards studies would confirm it.

What happens in the eating vegetables only and eating meat only feeding regimes probably depends a little on the exact composition of the meals and the insulin sensitivity of the individual.  But I would say that for both of these regimes, it is almost certain they will lose significant weight, and stay mostly healthy.  It is possible that a vegetable diet of almost exclusively starches and frequent meals, combined with someone who is highly insulin resistant, would result in constantly elevated insulin. This of course would result in some metabolic dysregulation, where energy expenditure is down regulated and insulin shunts some carbs into fat through de novo lipogenesis. I think this is unlikely to be what a vegetable only diet would look like.  It’s most likely that they will just lost weight.  They might not be that satisfied with their food, but all should be OK at least in the short term. In the longer term, B12, essential fatty acids, and amino acid deficiencies from vegetarianism should be considered.

Overall predictions for:

  1. Meat only diet – good weight loss, good energy, reasonable regulation of energy expenditure.  Need vegetables in the longer term for fiber and other micronutrients.
  2. Vegetable only diet – weight loss, although not as great as the meat only diet.  Some down regulation in energy expenditure depending on the metabolic health of the individual and the amount of starch eaten.  Not recommended long term because of lack of essential nutrients.

Now what we really want to consider is this one.  Someone eats just candy for six weeks. They are eating less than their daily energy requirements, so given you can’t defeat the first law of thermodynamics, then the weight loss should be predictable?

Not so fast I say.  I predict a few things will happen and the extent of this will depend on the metabolic health and the individual’s susceptibility to metabolic dysregulation.  This will depend on genes, age, and metabolic history.

So for the most insulin resistant person, a candy only diet will provoke constant hyperinsulinemia.  That is to say insulin, the fat storage hormone, will constantly be elevated. That means:

  • Fat burning is switched off
  • Carbs and fat are stored as fat
  • Energy expenditure is down regulated
  • Insulin probably blocks leptin, so they still feel constantly hungry

These factors can at least theoretically conspire to reduce energy expenditure and preferentially partition energy into fat. As time goes by, the sugar and fat combination in candy makes the insulin resistance and general metabolic dysfunction worse and worse.

My prediction is that it is possible to gain fat mass and therefore weight even on a calorie restricted diet because of the dysregulation that sugar provokes.

A good example of this in action is the OB OB mouse model. These are animals bred to be leptin deficient. That means they cannot send or receive a signal from the fat cells to down regulate hunger and to increase physical activity. That’s really the model which has shown us that leptin changes energy out and partitions energy into fat at the expense of other uses.

The thing is in humans, obese people become leptin resistant, which is a similar outcome to being leptin deficient.  Either way the brain can’t see leptin and down-regulate hunger and start expending not storing energy.

High insulin and the inflammatory pathways through sugar and so forth are highly implicated in leptin resistance.

In other words, I am saying that sometimes it is at least theoretically possible to eat a lot less and still get fat. The OB OB mouse eating exactly the same food as a normal leptin producing mouse gets obese, while the normal mouse stays lean. The OB OB mouse stops moving and stores a higher amount of food as fat.  When the OB OB mouse gets leptin injections it moves more and gets leaner.  The leptin injections have no effect on the lean mouse.

The solution? Stay off the junk carbs.

How ketogenic (low carb high fat) diets work

A really nice paper was just published by Paoli, Rubini, Volek and Grimaldi in the European Journal of Clinical Nutrition titled “Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets”

You won’t see a better review paper for summarizing the latest in how we think carbohydrate restriction affects various aspects of metabolic health; from weight loss to neurological issues to acne (yes acne!).

A second excellent review article was also published in Nutrition Today by Volek (again!) and Phinney, the low carb gurus. This one is called “A New Look at Carbohydrate-Restricted Diets: Separating Fact From Fiction”. Again this is an excellent scientific review paper.

What I should be doing in this blog is simply drawing your attention to this good work and you can go and check it out for yourself.

Except I’m aware that unless you work at a university, that’s easier said than done. You’d have to buy the papers, which means that most of the people who stand to benefit from the knowledge won’t.

Actually, copyright publishing is a scam of the highest order. What happens is that guys like Volek and Phinney put in heaps of work, often that work is paid for by either public institutions, or by research grants gained through public funds. They then (usually) slave away in the degrading process of blinded peer review, often having to respond to inane comments and endless rebuttals. When they are done, they then sign all of their IP over to a journal, which keeps it all for no cost (and all profit) in perpetuity. Can you imagine anywhere else in the business world that would happen besides academia? It’s laughable, but it is actually what happens to us academics everyday and frankly, we no longer find it funny.

Anyway, I digress. What I really want to do here is summarize the two reviews.

Let’s start with the Nutrition Today paper by Volek and Phinney, which is a nice synthesis of the available evidence for the biology of human energy regulation and homeostasis, and how a carbohydrate restricted diet operates. The main points here are:

  1. Saturated fat levels in the blood are not associated with dietary saturated fat intake, but dietary carbohydrate intake. They show evidence from both randomized controlled trials and population data for this.
  2. They discuss in detail what the keto-adapted (fat adapted) state is; how this comes about, including increased beta oxidation of fat, decreased hyperinsulinemia, and a reorchestration of substrate utilization in the body, including the use of ketones to fuel brain function. It is interesting that the majority of practicing dietitians, endocrinologists, cardiologists, and public health physicians have never heard of any of this.
  3. They point out what is a very important and obvious set of outcomes, which are well documented in the scientific literature; that treating a patient with insulin resistance with a low fat/high carb diet is palliative and going to make the problem worse. If you are having trouble getting glucose into your cells, then reduce the glucose load stupid!
  4. They show a nice little diagram, which I have reinterpreted and redrawn below, to show the role of dietary carbohydrate in metabolic (dys)function. To quote the authors “The major point is that SFA (saturated fatty acids), and the response to eggs, has a totally different metabolic behavior when consumed in the context of a low carbohydrate diet.”Slide1
  5. They show a meal plan for a typical low carb daily meal. This is excellent as it shows what real and tasty foods we are talking about.

2500 kcal daily food intake restricting carbs

Breakfast (scrambled eggs with sides of spinach and sausage)

  • Scrambled eggs: 2 large + 1 tbsp palm oil
  • Mozzarella cheese: 1 oz
  • Pork sausage: 2 links (48 g)
  • Chopped frozen spinach, boiled: 3/4 cup (142.5 g) + 1.5 tbsp butter

Snack

  • 1/2 Avocado: 67 g
  • Swiss cheese: 2 oz (56 g)

Lunch (broiled salmon and a side salad)

  • Broiled Atlantic salmon: 4 oz + 1 tbsp butter
  • Mixed baby greens: 2.5 cups
  • Diced tomatoes: 1/4 cup
  • Chopped onion: 1/8 cup
  • Feta cheese: 1 oz
  • Black and green olives: 4 each
  • Blue cheese dressing: 1.5 tbsp

Snack

  • Peanuts, oil-roasted: 1 oz
  • Hood Calorie Countdown milk: 1/2 cup

Dinner (sirloin with sauteed mushrooms and cauliflower ‘‘mashed” potatoes)

  • Beef sirloin tips: 3 oz
  • Olive oil: 1.5 tbsp
  • Sauteed mushrooms: 1/4 cup
  • Olive oil cooking spray
  • Cauliflower ‘‘mashed potatoes’’: boiled cauliflower 1 cup + shredded cheddar cheese 1 oz + Butter 1 tbsp
  • Sugar-free jello: 1/2 cup (121 g)

Macronutrients:

  • Protein: 134 g
  • Carbohydrates: 42 g, Fiber 20 g
  • Fat: 204 g
  • Cholesterol: 853 mg
  • SFA: 81 g
  • MUFA: 78 g
  • PUFA: 28 g

Reproduced from Volek and Phinney (2013), Nutrition Today

Now on to the second paper in the European Journal of Clinical Nutrition titled “Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets”. This is a comprehensive scientific review of the evidence and emerging evidence for the treatment and prevention of a range of chronic diseases with carbohydrate restricted (ketogenic) diets. I have adapted one of their figures into two new ones, showing the state of scientific evidence (strong and emerging separately) for “therapeutic uses of the ketogenic diet”. Hopefully these figures are self-explanatory.

I draw your attention to the “suggested mechanisms” under each one. I’m not going to go into these in detail but it is worth looking at these two figures and noting a few things:

  1. Carbohydrate restricted diets are a legitimate and well documented approach to the treatment of a wide range of issues.
  2. There are common mechanisms, mostly about reducing the load of insulin the body has to deal with. This is because the body has to dispose of less dietary carbohydrate. This point is seemingly lost on most in the field of chronic disease prevention and treatment. Hyperinsulinemia is a problem in itself, reducing it helps.
  3. As well, there are associated mechanisms associated with high insulin. There are problems in the IGF pathway, mitochondrial function, and inflammation.

Slide1

Slide2

There is now strong evidence to show that low carbohydrate diets are safe and effective treatments for several conditions, and have some likely positive effects for other conditions.

So that’s it. Two great papers. Hopefully I have captured the essence of what they are saying and where the evidence is at. This is important to get out there into the public and health community. While it’s all behind the paywalls of journals it won’t. So hopefully this helps.

Why some people must restrict carbs

Spot the difference
OK, I will start this by saying that this is a more academic piece about metabolic control in type 2 diabetics, and the ethics of feeding them low fat diets. It is a bit technical in places and deals directly with original research. Read on if you are interested!
The key message is that in my opinion, when you are insulin resistant, really the first option you should consider is restricting carbs. I hear a lot about “it’s the processed carbs, not the starchy veges that are the problem”, that “vegetarian and vegan approaches are good at reversing type 2 diabetes”, that “fibre solves everything” and so on.
Look, I agree that healthy humans can eat a wide variety of macro-nutrients that may contain plenty of carbs and nothing adverse will happen, but it’s likely that processed carbs will help metabolically well regulated healthy people into insulin resistance and a downward cycle of getting fatter and sicker. The mechanisms by which fructose (sucrose – table sugar is half fructose) work are being understood more clearly by modern science. The way fructose stirs up inflammation, blood lipids, liver fat deposition, addictive pathways in the mesolimbic system in the brain, and causes leptin resistance (the off switch hormone) are all important factors.
Once, or if, you become insulin resistant, I believe that macro-nutrient profiles are very important. Mainly, I am talking about restricting dietary carbs. Remember, if you are insulin resistant then you will have a problem getting dietary carbohydrate into your cells. The pancreas needs to produce more insulin to help do this. In the early stages of insulin resistance, all this means is you end up being hyperinsuliemic – having constantly high insulin – if you eat even moderate amounts of any dietary carbohydrate.
Hyperinsulinemia is known to have multiple direct and indirect effects on the body, making things significantly worse. Insulin is directly inflammatory. Insulin turns off fat oxidation and promotes fat storage and conversion of carbs into fat (de novo lipogenesis). Insulin probably blocks the hormone leptin in the brain (off switch not working again!). High insulin is directly implicated in many cancers, especially breast and prostate cancers. The list is growing all the time as we understand more about this essential hormone, which causes havoc when out of whack.
Interestingly, the treatment approach of most endocrinologists, dieticians and diabetes specialists is to advise those with insulin resistance to have a low fat, moderate protein, high fruit and vegetable diet. Taken correctly, and iso-calorically for weight maintenance, for even consistent small weight loss, this wil be a moderate or high carbohydrate diet. True, the carbs have some fibre and you could avoid all processed carbs. Nonetheless, it is overall carb load that is important here for the insulin resistant person.
Here’s the kicker – some of the “best” carbs recommended for these people by health professionals, because they are low glycemic index, don’t help. This is because these carbohydrates are absorbed slowly into the system; but because the insulin resistant person is so easily overwhelmed by even moderate carb loads, the result is day-long hyperinsulinemia. There’s plenty of evidence for this too.
The evidence comes, in the main, from feeding studies comparing normal metabolically functioning people, with type 2 diabetics.
Here are a few examples:
1. First, I have written about this before in less detail, the study with beans and glucose. The main thing about this paper is that it compares diabetics with healthy non-diabetic controls. This is very important to see the differential insulin response provoked by the same carb load. This study shows how the insulin responses to several types of beans are high and prolonged for Type 2 diabetics compared with controls.
2, This study in Diabetic Medicine in 1989 shows how rolled oat meals in diabetics result in massive hyperinsulinemia and hyperglycemia compared to the healthy controls after 3 hours. It seems to me that any of these meals are the last thing you would want to feed to a Type 2 diabetic.
Rasmussen et al (1989). Postprandial glucose and insulin responses to rolled oats ingested raw, cooked or as a mixture with raisins in normal subjects and type 2 diabetic patients.
Cooking and processing of food may account for differences in blood glucose and insulin responses to food with similar contents of carbohydrate, fat, and protein. The present study was carried out to see if short-term cooking of rolled oats caused an increase in blood glucose. Furthermore, we wanted to see if dried fruit could substitute for some of the starch without deterioration of the postprandial blood glucose response. We therefore compared the blood glucose and insulin responses to three isocaloric, carbohydrate equivalent meals in 11 normal subjects and 9 Type 2 diabetic patients. Meals composed either of raw rolled oats, oatmeal porridge or a mixture of raw rolled oats with raisins were served. In normal subjects, the three meals produced similar glucose (75 +/- 22, 51 +/- 16 and 71 +/- 23 (+/- SE) mmol l-1 180 min, respectively) and insulin response curves (3160 +/- 507, 2985 +/- 632 and 2775 +/- 398 mU l-1 180 min, respectively). Type 2 diabetic patients also showed similar postprandial blood glucose (515 +/- 95, 531 +/- 83 and 409 +/- 46 mmol l-1 180 min, respectively) and insulin (5121 +/- 850, 6434 +/- 927 and 6021 +/- 974 mU l-1 180 min, respectively) responses to the three meals. Thus, short-term cooking of rolled oats has no deleterious effect on blood glucose and insulin responses, and substitution of 25% of the starch meal with simple sugars (raisins) did not affect the blood glucose or insulin responses.
3. Here’s another paper in Diabetes Care from 1987. In this study they fed diabetics 50g of starch contained in various foods. The foods were neither isocaloric, nor matched for other marco-nutrients (see table). The insulin response was greater for many of the foods than predicted by the glucose response. There were no comparison controls though.
fig 3
The glucose and insulin areas under the curve are shown below. A few comments – while the lentils and kidney beans provoked a lower peak glucose, the rise took longer and the response was still increasing at 2 hours. Second, the results show that all foods produced hyperinsulinemia for several hours afterwards.
Untitled
fig2.1
4. And then this paper in Diabetes Care from 1998. Look at the insulin curve responses to three different meals below – a standard American meal, a low starch/high fibre meal, and a high starch meal. You’ll notice a few things. First, the subjects are hyperinsulinemic after all meals. Second, the low starch meal appears to do much better than the higher starch meal. This research is flawed because the macronutrient compositions of the two meals are different – so it’s not the carbs that define the different insulin responses. There are no healthy controls either – so who knows what the difference is between meals and insulin resistant/insulin sensitive subjects.
The “high starch” diet is 55% carbs, 15% protein, and 30% fat. The “low starch” meal is 43% carbs, 22% protein, and 34% fat. So we see here that people have better insulin responses on lower carb, higher protein, higher fat diets! Just reduce the carbs a bit more and you might have something that resembles a healthy diet for a Type 2 diabetic. Another example of poorly conducted research reaching the wrong conclusions about dietary carbs.
5. Finally, heres a paper in the Archives of Internal Medicine from 2005. The figure shows the day long insulin response of the same subjects (they are their own control) on a low carb diet. The low carb diet is ketogenic. To be fair, the diets are not isocaloric because the subject spontaneously ate less food, as is usual for a low carb diet. They were not restricted and ate to fullness though.
Boden-Insulin51
Take home message:
If you are insulin resistant, you are by definition carbohydrate intolerant. Conventional treatment is to reduce fat, eat less processed carbohydrate, but still at least a moderate carb diet. That will result in chronic hyperinsulinemia and make things worse. The best and most sustainable approach is to restrict carbs and to eat moderate protein with fat as needed to fill you up. You can achieve the same result on a vegan diet or a vegetarian diet, it doesn’t matter, although more difficult. I would hypothesize that any diet in which the symptoms of diabetes are reversed is a carb restricted diet, whether it be through carb retsriction alone or an overall very low calorie diet.
Call to action? Understanding that dietary carbs affect some people very negatively is very important but not understood at all by mainstream medicine. Start telling your doctor about this! Pass on this blog, email people, get on Facebook or Twitter – do what you can. This will be a ground up movement in changing public health nutrition.

Will sweeteners make you fat or sick?

sweeteners

Now here’s a very controversial topic: aspartame and other artificial sweeteners. My conversations with (usually) men on sugar and substitutes usually go something like this:

Me: ‘Have you thought about replacing your fizzy drinks with diet drinks like Coke Zero or Diet Coke?’

‘No.’

Me: ‘Why not?’

‘I don’t drink that shit.’

Me: ‘What do you mean?’

‘It’s full of that artificial crap, like those sweeteners and other chemicals. They cause cancer. Diet Coke is a girls’ drink, as well.’

Me: ‘So you’d rather drink that 500 ml of Coke, which has 12 teaspoons of sugar in it?’

‘Yep.’

Me: ‘Even though half of that Coke will send your blood sugar through the roof, raise your insulin, and leave you hungrier than before you had it, while the other half that is fructose will go straight to your liver and screw you up in several other ways? And even though there is no evidence for negative outcomes, especially cancer, in the artificial sweeteners like aspartame, one of the most tested and long-standing additives to the human food supply?’

‘What are you talking about, [usually some profanity starting with d or f and ending with -head]?’ (Returns to drinking, laughing at me.)

Okay, my overall approach was probably fundamentally flawed and really misses the mark on the ‘how to win friends and influence people’ scale, but this is very typical of the responses I hear from men. I’m not a promoter of diet drinks for their own sake, but if you want a sweet drink I think the choice is a no-brainer. Sugary drinks – and fruit juice is in this category as it contains exactly the same amount of sugar as regular Coke – are a worse choice than a diet drink. Sugar is relatively toxic to the body. Aspartame is probably not.

What the heck does “probably not” mean? That’s a very good question. The answer is that there isn’t much evidence, especially experimental evidence with humans, showing adverse health outcomes.

Don’t you hate it when researchers sit on the fence and say that sort of stuff? There isn’t convincing evidence that sweeteners don’t harm you either. So it’s a double edged sword. The reality is that you would be better off drinking water. But that’s not the social and environmental reality of the world we live in. I’m saying that all things being equal, I’d prefer the diet drink to the full sugar version.

OK, I hear all the paleo, whole foods guys screaming – and I hear you. But how do you balance that approach with the pragmatism of public health? (clue: think about our approaches to reducing smoking which is obviously bad for you).

Here’s why I would take a more pragmatic approach to sweeteners. First, all foods are made of chemicals. Nutrients are chemicals. Too much or too little of any nutrient has adverse effects. In other words, when we exceed our biological capacity to deal with a nutrient it is almost always a problem. This is why high carb diets are a problem for some people. Aspartame, when synthesised, breaks down into phenylalanine (an amino acid), aspartic acid, and methanol – all of which are found naturally in foods. So I think it’s a matter of perspective and harm with sweeteners. We can deal with these substances in small amounts.

This isn’t everyone’s view, but I think there is now enough evidence to make this recommendation a public health one. In other words, on the continuum of water being the best and sugary drinks the worst, sweetened drinks and meals fit somewhere in between. That’s different than a personal health choice. It might be considered “harm minismisation”. Some people will say that by drinking sweet (even artificially sweetened) drinks you are giving people a taste for sweet stuff. My response is that we already like sweet stuff and no amount of abstinence from sugar will completely cure our taste for it. That being said, lower carb, sugar free diets do go a long way to curing the actual addition many people develop. Through sweeteners, food technology allows us to enjoy sweetness without the sugar.

Besides aspartame, which can have an aftertaste that some people find off-putting (and was originally developed as a fly spray which is even more off putting), there are two other popular sweeteners available in New Zealand: Splenda and Stevia.

Splenda is sucralose, which is made from sucrose (normal sugar), but with a refining process that reduces the calories. Because sucralose is inert (not metabolised) in the body it is calorie free. This product looks and feels a bit more like actual sugar and doesn’t have the same aftertaste as aspartame sweeteners, so it is much better for cooking and baking.

Stevia is a natural plant extract. In New Zealand it is sold under the name Sweete in 2 g sachets, which contain 1 calorie. Compared with sugar, the onset and duration of sweetness is slower and longer. Stevia is, however, about 16 times sweeter than sugar, the 2 g sachet providing the same sweetness as a teaspoon of sugar. So if you are worried about being natural, this plant-extract additive is pretty good.

On balance, I much prefer the Stevia sweetener.

A few comments about research on these sweeteners:

  1. None are likely to stimulate an insulin response on their own.
  2. I acknowledge that actual experimental trials with these substances on humans will never happen because that research is unethical. So we are left with only some prospective study showing no harm. That’s not that convincing.
  3. A study out last week in the journal “Diabetes Care” showed something very interesting. The paper by Pepino et al was entitled “Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load“. So you can see from the title that Sucralose (Splenda), although on its own doesn’t stimulate an insulin response, combined with glucose does magnify the glycemic and insulin response and area under the insulin curve. That’s interesting. I have no idea why that would happen, whether it happens with other sweeteners, how much glucose is required for this response, or whether it applies in slimmer subjects (average BMI was 42). In any case, it is a bit of a warning about Splenda in particular. Not sure about the others.
  4. Watch out for emotional claims about research in this space. Here’s a great example of one about the above paper which is titled “Splenda and Sucralose shown to contribute to the development of diabetes“. That seems to happen all the time in this field. Let’s agree that absence of evidence isn’t the same as evidence of absence. But let’s also agree that the evidence just isn’t their yet for the outright harm of these substances.

So will they make you fat and sick? They might, but sugar is more likely to do so. Are they harm free? Probably not entirely, but in an obesity epidemic let’s be pragmatic in public health.

What do I actually eat?

CIMG1034

Grant Schofield has a chat to a village pig about the pig’s future. The pig listens carefully.

Thanks to everyone who has started following this blog.  Frankly, while I find this stuff interesting and important, I had no idea that it was shared by so many other people.  An academic’s real-life exposure to social media is an eye opener and fun. 3000 hits in a little over a week!

So the main question I have had from people so far is “what do you eat?” and “what about kids?” I think I can talk about both of those, in this and the next post. After all I am me, and I am the father of three boys.

Some background:

I have been active and relatively fit my whole life, including a stint as a professional triathlete. One observation and my main excuse for not being a long lasting and super duper fast professional triathlete, was that I could never get my weight under 85-86 kg.  In fact, when I did my fastest time in Ironman NZ 2001, I was officially entered in the heavy weight “clydesdale” division, where I was 94 kg at weigh in. To be fair, that was at the conclusion of the pre-race pasta party. My time of 9:04 was (I claimed at least), at the time, a clydesdale world record.  I’m not sure there is such a record but it gave me mileage at the time – “world’s fastest fat guy over the Ironman triathlon distance”.

What bugged me though was why I couldn’t get fully race lean. I was eating low fat, high carb.  It was exactly what the experts said I should do.  I could hardly exercise any more.  I was training up to 25 hours a week! In fact, I noticed the same thing when I watched the Ironman in Taupo New Zealand  this year.  Roughly one third of the field is overweight or obese in my judgement.  How can they stay fat doing so much exercise?  Maybe they are LESS fat than when they started?  Or maybe their high carb diet and chronically raised insulin fails to allow fat burning?

Anyway, post triathlon retirement and children arriving I was up over 102 kg.  I was still exercising everyday, eating “healthily” and still fatter than ever and it was getting out of control.  Why was I always hungry? Why did my energy always “fall of a cliff” after lunch? I was trying really hard to NOT be a fat bastard. You can imagine, I do physical activity, nutrition, and obesity research.  You lose street cred when you are fat.

My Solution:  Take up marathon running and starve myself.  This method got the weight off. It also made me sick and injured.  I was especially prone to colds and flu with several every year. I hate flu.

I finally got consistently injured enough to flag the running and take up age group triathlon again. Same results:  weight creeping, always creeping.  When it crept past an acceptable point, I’d starve myself and exercise like crazy.  I’d get sick.

Surely there has to be a better way? Enter, LCHF.

Now: I’m down to my lightest weight since mid-high school.  79 kg, lean, full of energy, and all the  injury and illness has gone.  I’m eating until full, as much as I like.  It’s Awesome.  I wouldn’t have believed this was possible.  But it is.

I started reading all the literature and science in nutrition, which has been part of my broader field for a while.  I have read enough now and experienced enough case work to change my starting hypothesis.

That’s partly why this blog is here.  That’s why I have changed my research and practice direction in physical activity, nutrition and obesity, as well as the broader area of well being. I am now up with the science and we need to do it better.

So what do I eat?

I don’t always eat three meals a day now. I often try intermittent fasting which usually isn’t planned but happens naturally* according to hunger, food availability, work pressures and convenience. For this to be possible is a revelation to me.  I have spent almost all of my life being pretty much hungry the whole time.  If I didn’t eat every few hours I would fall off a glucose cliff and basically become 50% functional.  This is hardly convenient and hardly optimal for a high performance life.  My new way of eating also allows me to easily create calorie deficits to manage my weight if I feel I need to.

*The fact that I can quite often end up fasting accidentally for relatively long periods, while staying mentally sharp and full of physical energy, is an amazement to me.  I’ve spent my whole life doing exactly the opposite.  It’s sort of like the “user manual” for being me has been found.  I am fat adapted and can oxidize fat as a primary fuel source. I can use ketones as a fuel for my brain.  I don’t fall off the glucose “cliff” every few hours.  This is a great place to be in.  It also means you lose the cravings for the sweet food, especially sugar. This is the main benefit most people I know who have moved into this style of eating report. The constant energy and loss of ridiculous hunger every few hours.

I also have the occasional off day or meal when I just do whatever I feel like.  We are all human after all.  I used to plan these for a while and really looked forward to them.  Frankly, now, I can do this if I want but I feel so crappy after eating simple carbs, especially wheat products, that I just don’t bother much.  Again, this is a revelation as my self control in the face of high sugar high carb foods in the past has been completely non-existent!

Here are some typical meals for me:

Breakfast

  • Scrambled eggs with whipping cream and streaky farm bacon from the butcher fried in coconut oil
  • Smoothie made with coconut cream or milk, whipping cream, coco powder and or fresh berries
  • Salmon, avocado and tomato
  • Omelette with cheese and veggies (meat added when I feel like it).

Lunch

  • Massive salad with lettuce, tomato, capsicum, cucumber, cheese, meat of some sort – fish, chicken, bacon whatever is around, avocado, almonds.  Mix up and add copious amounts of dressing which is home made olive oil and vinegar or mayo.  The dressings have to be made by you, because almost all commercial dressings use hydrogenated vegetable fats – yuck – and are often high in sugar
  •  That’s my “go-to” lunch above.  I lack imagination for lunch according to my family, but that’s the way it goes!  I do have eggs and smoothies for lunch sometimes or something from the dinner/lunch list below.

Dinner

  • Some sort of meat or fish.  Heaps of veggies (green and red veggies as a rule, cauliflower is also good, avoid starchy ones). I like pork with crackling. This is the time to really appreciate the flavors of fat.
  • Wine, although I am trying an alcohol free month right now because it was getting out of hand!
  • Berries and cream for dessert
  • Low carb cheese cake is a favorite

Other tips and traps

  1. Don’t trim fat. Healthy fats are monounsaturated olive and other nut oils, Omega 3 fish oils, and healthy meat fats (unprocessed red and white meats including beef pork, fish and chicken), as well as dairy fats. Coconut oil is great.  Avoid hydrogenated and polyunsaturated fats, especially in cooking.
  2. Just to reiterate, you have to replace carb and protein calories with something.  The only macronutrient left is fat.  Our ancestors likely coveted fat.  Fat, at least as far as insulin and leptin goes, is metabolically benign.  Carbs are not, especially when they are rapidly absorbed.
  3. Coffee is OK, I use whipping cream not milk. I tend to avoid dairy except cheese of all sorts (yum!) and cream.  Milk can be high in lactose (a carbohydrate). Those who are more carbohydrate tolerant (have an ability to eat carbs without weight gain) can go for full fat milk and a fuller range of dairy. Most kids are in this  category.
  4. Alcohol is a tricky question.  Alcohol is certainly not metabolically benign.  I recommend abstinence during the adaptation period into LCHF. Have a look at this link to explore more about keto/low carb adaptation. Then what you want is a low carb drink if you enjoy alcohol.  I certainly don’t drink alcohol for physical health reasons but I do drink it for social and marital health reasons!  My wife Louise and I spend lots of time sitting on our deck drinking wine and talking.  Great fun!  The active alcohol is called ethanol and is processed in the liver without much effect on insulin, at least not directly. It in fact follows a similar and dangerous path to the liver and beyond.  It’s metabolically active in an inflammatory and insulin resistance-promoting kind of way.  However, that said, we all have our vices, the actual insulin raising carbs in a glass of wine are between 3 and 6 g, depending on the wine and the size of glass (we have big glasses in our house!) so a glass or two is fine. Beers have way more carbs (12-20 g) per bottle and contain wheat that may result in other metabolic effects for some people.  You can get low carb beers of course.  I don’t really care for spirits, as a result of bad youth experiences I think, but if you do use them then it’s crucial to leave out the sugar based mixers.

That’s my wrap.  I’m not perfect and as a normal human fall off the wagon too.  I’m on the 18/21 plan. If there are 21 meals in a week, try for at least 18 good ones, hopefully better.  Let me know your favorite meals and we can post them up.


What do I actually eat?

CIMG1034

Grant Schofield has a chat to a village pig about the pig’s future. The pig listens carefully.

Thanks to everyone who has started following this blog.  Frankly, while I find this stuff interesting and important, I had no idea that it was shared by so many other people.  An academic’s real-life exposure to social media is an eye opener and fun. 3000 hits in a little over a week!

So the main question I have had from people so far is “what do you eat?” and “what about kids?” I think I can talk about both of those, in this and the next post. After all I am me, and I am the father of three boys.

Some background:

I have been active and relatively fit my whole life, including a stint as a professional triathlete. One observation and my main excuse for not being a long lasting and super duper fast professional triathlete, was that I could never get my weight under 85-86 kg.  In fact, when I did my fastest time in Ironman NZ 2001, I was officially entered in the heavy weight “clydesdale” division, where I was 94 kg at weigh in. To be fair, that was at the conclusion of the pre-race pasta party. My time of 9:04 was (I claimed at least), at the time, a clydesdale world record.  I’m not sure there is such a record but it gave me mileage at the time – “world’s fastest fat guy over the Ironman triathlon distance”.

What bugged me though was why I couldn’t get fully race lean. I was eating low fat, high carb.  It was exactly what the experts said I should do.  I could hardly exercise any more.  I was training up to 25 hours a week! In fact, I noticed the same thing when I watched the Ironman in Taupo New Zealand  this year.  Roughly one third of the field is overweight or obese in my judgement.  How can they stay fat doing so much exercise?  Maybe they are LESS fat than when they started?  Or maybe their high carb diet and chronically raised insulin fails to allow fat burning?

Anyway, post triathlon retirement and children arriving I was up over 102 kg.  I was still exercising everyday, eating “healthily” and still fatter than ever and it was getting out of control.  Why was I always hungry? Why did my energy always “fall of a cliff” after lunch? I was trying really hard to NOT be a fat bastard. You can imagine, I do physical activity, nutrition, and obesity research.  You lose street cred when you are fat.

My Solution:  Take up marathon running and starve myself.  This method got the weight off. It also made me sick and injured.  I was especially prone to colds and flu with several every year. I hate flu.

I finally got consistently injured enough to flag the running and take up age group triathlon again. Same results:  weight creeping, always creeping.  When it crept past an acceptable point, I’d starve myself and exercise like crazy.  I’d get sick.

Surely there has to be a better way? Enter, LCHF.

Now: I’m down to my lightest weight since mid-high school.  79 kg, lean, full of energy, and all the  injury and illness has gone.  I’m eating until full, as much as I like.  It’s Awesome.  I wouldn’t have believed this was possible.  But it is.

I started reading all the literature and science in nutrition, which has been part of my broader field for a while.  I have read enough now and experienced enough case work to change my starting hypothesis.

That’s partly why this blog is here.  That’s why I have changed my research and practice direction in physical activity, nutrition and obesity, as well as the broader area of well being. I am now up with the science and we need to do it better.

So what do I eat?

I don’t always eat three meals a day now. I often try intermittent fasting which usually isn’t planned but happens naturally* according to hunger, food availability, work pressures and convenience. For this to be possible is a revelation to me.  I have spent almost all of my life being pretty much hungry the whole time.  If I didn’t eat every few hours I would fall off a glucose cliff and basically become 50% functional.  This is hardly convenient and hardly optimal for a high performance life.  My new way of eating also allows me to easily create calorie deficits to manage my weight if I feel I need to.

*The fact that I can quite often end up fasting accidentally for relatively long periods, while staying mentally sharp and full of physical energy, is an amazement to me.  I’ve spent my whole life doing exactly the opposite.  It’s sort of like the “user manual” for being me has been found.  I am fat adapted and can oxidize fat as a primary fuel source. I can use ketones as a fuel for my brain.  I don’t fall off the glucose “cliff” every few hours.  This is a great place to be in.  It also means you lose the cravings for the sweet food, especially sugar. This is the main benefit most people I know who have moved into this style of eating report. The constant energy and loss of ridiculous hunger every few hours.

I also have the occasional off day or meal when I just do whatever I feel like.  We are all human after all.  I used to plan these for a while and really looked forward to them.  Frankly, now, I can do this if I want but I feel so crappy after eating simple carbs, especially wheat products, that I just don’t bother much.  Again, this is a revelation as my self control in the face of high sugar high carb foods in the past has been completely non-existent!

Here are some typical meals for me:

Breakfast

  • Scrambled eggs with whipping cream and streaky farm bacon from the butcher fried in coconut oil
  • Smoothie made with coconut cream or milk, whipping cream, coco powder and or fresh berries
  • Salmon, avocado and tomato
  • Omelette with cheese and veggies (meat added when I feel like it).

Lunch

  • Massive salad with lettuce, tomato, capsicum, cucumber, cheese, meat of some sort – fish, chicken, bacon whatever is around, avocado, almonds.  Mix up and add copious amounts of dressing which is home made olive oil and vinegar or mayo.  The dressings have to be made by you, because almost all commercial dressings use hydrogenated vegetable fats – yuck – and are often high in sugar
  •  That’s my “go-to” lunch above.  I lack imagination for lunch according to my family, but that’s the way it goes!  I do have eggs and smoothies for lunch sometimes or something from the dinner/lunch list below.

Dinner

  • Some sort of meat or fish.  Heaps of veggies (green and red veggies as a rule, cauliflower is also good, avoid starchy ones). I like pork with crackling. This is the time to really appreciate the flavors of fat.
  • Wine, although I am trying an alcohol free month right now because it was getting out of hand!
  • Berries and cream for dessert
  • Low carb cheese cake is a favorite

Other tips and traps

  1. Don’t trim fat. Healthy fats are monounsaturated olive and other nut oils, Omega 3 fish oils, and healthy meat fats (unprocessed red and white meats including beef pork, fish and chicken), as well as dairy fats. Coconut oil is great.  Avoid hydrogenated and polyunsaturated fats, especially in cooking.
  2. Just to reiterate, you have to replace carb and protein calories with something.  The only macronutrient left is fat.  Our ancestors likely coveted fat.  Fat, at least as far as insulin and leptin goes, is metabolically benign.  Carbs are not, especially when they are rapidly absorbed.
  3. Coffee is OK, I use whipping cream not milk. I tend to avoid dairy except cheese of all sorts (yum!) and cream.  Milk can be high in lactose (a carbohydrate). Those who are more carbohydrate tolerant (have an ability to eat carbs without weight gain) can go for full fat milk and a fuller range of dairy. Most kids are in this  category.
  4. Alcohol is a tricky question.  Alcohol is certainly not metabolically benign.  I recommend abstinence during the adaptation period into LCHF. Have a look at this link to explore more about keto/low carb adaptation. Then what you want is a low carb drink if you enjoy alcohol.  I certainly don’t drink alcohol for physical health reasons but I do drink it for social and marital health reasons!  My wife Louise and I spend lots of time sitting on our deck drinking wine and talking.  Great fun!  The active alcohol is called ethanol and is processed in the liver without much effect on insulin, at least not directly. It in fact follows a similar and dangerous path to the liver and beyond.  It’s metabolically active in an inflammatory and insulin resistance-promoting kind of way.  However, that said, we all have our vices, the actual insulin raising carbs in a glass of wine are between 3 and 6 g, depending on the wine and the size of glass (we have big glasses in our house!) so a glass or two is fine. Beers have way more carbs (12-20 g) per bottle and contain wheat that may result in other metabolic effects for some people.  You can get low carb beers of course.  I don’t really care for spirits, as a result of bad youth experiences I think, but if you do use them then it’s crucial to leave out the sugar based mixers.

That’s my wrap.  I’m not perfect and as a normal human fall off the wagon too.  I’m on the 18/21 plan. If there are 21 meals in a week, try for at least 18 good ones, hopefully better.  Let me know your favorite meals and we can post them up.


Diet wars: Can you really eat fat and get lean?

Grant Schofield doing the weekly LCHF shopping sans vegetables
Grant Schofield doing the weekly LCHF shopping sans vegetables, still to be purchased

There’s a food fight cooking…

In the red corner, we have the national nutrition guidelines, with its support crew of dietitians and most of the conservative medical and scientific community. They are the reigning public health champions. They are undefeated, but then they haven’t been seriously challenged. Until now.  In the blue corner, we have a new challenger. He’s been around a while but till now he’s just been shadow boxing. For some reason he strikes fear in those around him. I present to you…..Fat.

We’ve been told for decades now that saturated fat is the major enemy in the battle against obesity and chronic disease. Reduce your fat intake and eat more carbs instead we’re told.  Carbs are essential for human health we’re told.  Eat less, move more we’re told and you’ll stay in shape.  Here are the National Nutrition guideline for New Zealand.:

  1. Maintain a healthy body weight by eating well and by daily physical activity.*
  2. Eat well by including a variety of nutritious foods from each of the four major food groups each day:
  • Eat plenty of vegetables and fruits.
  • Eat plenty of breads and cereals, preferably wholegrain.
  • Have milk and milk products in your diet, preferably reduced or low-fat options.
  • Include lean meat, poultry, seafood, eggs or alternatives.
  1. Prepare foods or choose pre-prepared foods, drinks and snacks:
  • with minimal added fat, especially saturated fat
  • that are low in salt; if using salt, choose iodised salt
  • with little added sugar; limit your intake of high-sugar foods.

As well:

  1. Drink plenty of liquids each day, especially water.
  2. If choosing to drink alcohol, limit your intake.
  3. Purchase, prepare, cook and store food to ensure food safety.

* At least 30 minutes of moderate intensity physical activity on most if not all days of the week and if possible add some vigorous exercise for extra health and fitness.

Yep, that’s the advice and what I have been preaching publicly for the last 15 years, and practicing privately for my whole adult life.

So what’s the problem? The guidelines seem sensible right?  They’re evidence based, and the evidence is extensive right? Yes, sort of, and no.

Let’s deal with the Yes’s first:

Yes, there is extensive and compelling evidence that the type of diet described above is better for you than the Standard American Diet, henceforth known as the SAD :(.  This evidence is from randomized controlled trials, detailed longitudinal studies, and correlational studies.  There are plausible and known mechanisms for some of it, especially whole foods and meats. The important and convincing data around exercise and health is reflected in the guidelines too.

But that’s compared to the SAD.  It’s like saying that because studies show that smoking filtered, low tar cigarettes results in better health, less lung cancer, stroke, and heart disease than smoking roll your own cigarettes, that we should all smoke low-tar cigarettes. Bogus logic. 

The Sort Of’s

  • Sort Of: The part about maintaining a healthy body weight is true – that is good for you. And eating healthily certainly is the way to do this. A low fat diet could make this possible but in the 18 randomized controlled trials to date, where low fat diets have been pitted against low carb high fat (LCHF) diets, there is no instance where the low fat diet has outperformed the LCHF diet. Weight loss and risk profiles, including lipids, are all better with the LCHF. It’s been a knockout in every fight so far.
  • Sort Of: Salt raises blood pressure simply by increasing blood volume.  Equally, low salt is a risk for insulin resistance. Anyone who has ever completed a well formulated LCHF diet is aware of the importance of salt supplementation to prevent low blood pressure and cramps. The same is true for indigenous cultures who eat LCHF diets; they all add about 1.5-2.0 g salt a day.

The No’s

  • No: Where is the convincing evidence to say that saturated fat on its own is a health risk?  Here’s a recent meta-analysis of the longitudinal studies in the American Journal of Clinical Nutrition. There is no evidence of an association between saturated fat intake and cardiovascular outcomes in a combined cohort of more than 347,000 adults followed up for between 5 and 25 years.
  • No: Eat plenty of breads and cereals, preferably wholegrain, and limit your intake of high-sugar foods. Really? How about going with the more plausible mechanism for how we store fat in fat cells via raised insulin.  Insulin, you recall, is raised by carbs, even the so called healthy whole grains.  Sugar is an extra baddie – we all agree on that.  But the language is so lame, it almost condones anything other than high sugar.  Sugar and other insulin raising carbs promote hyperinsulemia, inflammation, glycation, oxidative stress, and fat storage. Because the inevitable outcome of a low fat diet is either starving yourself and keeping insulin under control that way, or a high carbohydrate diet. Either way, this regime is neither sustainable nor healthy in the long run. A low fat diet with sufficient calories for normal living is going to have to also be a high carb diet. Even if you eat lots of extra protein to avoid the extra starchy carbs, you end up with glucose anyway because excess protein will be converted, albeit inefficiently, into glucose in the liver via gluconeogenesis. 
  • No: A calorie is not a calorie.  Calories from different sources have profoundly different metabolic and hormonal effects in the body. Starchy and easily digested carbs raise insulin and insulin chronically blocks leptin. Protein raises insulin but the effect is short lasting and therefore satiating.  Fat is metabolically benign in the absence of chronically elevated insulin. This is why an “eat as much as you feel like” LCHF diet out-performs a low fat high carb diet. The way you get weight homeostasis is by controlling insulin. Perversely, the healthy food guidelines most governments push are likely to negatively affect the people who are highest risk the most; i.e. those who are less carbohydrate tolerant and therefore predisposed to excessive weight gain and insulin resistance in the presence of high carb diets. 

In the end, it looks a bit like the story about the time I was in a long distance ocean swim. The support kayaker taps me on the shoulder and says “You are going to need a change of strategy”.  “Why, I’m swimming flat out already” I reply.  “Because you haven’t made forward progress in an hour, in fact I think you are going backwards….”.  “I see, let’s talk about our options” I say.

We have to accept that we are making no progress in reducing the epidemic of obesity and chronic disease and we need to consider why. We need a discussion about our strategy.  This is the start of that discussion. We all agree that our industrialized food supply is bad but we don’t agree on how to change it and what nutrients are causing the damage.  We all mostly agree that sugar is a bad guy, but we can’t all agree that it is the effect of sugar on insulin and insulin resistance that is the problem. Yes sugar has fructose as well which has problems through other pathways. But, whether it’s loads of insulin-raising simple or complex carbs, it doesn’t matter – both need to be given the boot from the healthy food guidelines. In fact, perversely in my view, we ignore the fact that obesity is a metabolic disorder caused by any type of carb.  Sure, trans fats and the like don’t help. But let’s name the real VILLAIN here and now. It’s not saturated fat….it’s high carbs.

So what’s the answer?

  1. Stop doing nutrition research which tests one thing – the low fat dogma against the SAD. This is fundamentally bogus.
  2. Start doing research which has a start point in biology and evolution by natural selection.  That means start with some sort of paleo/primal LCHF as the “probably healthiest option” hypothesis.  Humans are omnivores = we eat plants and meat.  In human evolution, insulin was hardly ever raised excessively, and if it was, it was probably near the end of summer when man needed to pack away fat to survive the winter.
  3. Stop pretending we know everything about nutrition.  We don’t and we shouldn’t trust anyone who says they do. It’s a science in its infancy with a good deal of poor research behind it and an industry which has infiltrated research and public policy for its own benefit and not ours.
  4. Start to consider that like many other instances in human history, almost the opposite of what we have preached might be true.  Think Galileo, Hormone Replacement Therapy, causes of stomach ulcers, and dozens of times when medicine had it completely wrong.  It’s obvious that at least a few of the assumptions behind current healthy eating guidelines are bogus.

If you end up eating too many carbs in the presence of fat, no matter how paleo plant and meat based the rest of your diet, then all bets are off, you will get fat.

I’m writing this expecting to draw the wrath of colleagues, academia, government and medical and research conservatism. Hopefully first though they carefully consider points 1-4 above. What we need to start with is good science. I could be wrong, but so could you.

So let the diet wars commence; we’re in the ring and we’re ready to fight. We’re starting with the hypothesis that carbs make you fat, and that fat keeps you lean.  Bring it!

Footnote: There are typically three types of diet commonly and currently discussed; the LCHF diet, a low fat high carb diet and a moderate fat moderate carb diet (SAD). I want to reiterate that the SAD is the deadliest. A well formulated LCHF diet is not high protein, it is only adequate protein.  Low carb has nothing to do with dietary percentages.  It’s a total carb intake of <100g/day, maybe even <50g/day, or up to 150g/day for athletes. The LCHF approach is often confused by researchers and clinicians because I often see this regime criticised as either high protien, high fat, or the maount of carbohydrate quoted being far too high. Total daily carbs are what are important.

Thanks again to Helen Kilding in writing this blog

How to become a fat burning machine, lessons from athletes

Grant Schofield

Why become a fat burner?

In a previous post, Why some people stay skinny and others get fat I talked about how high carb foods lead to high insulin levels which effectively turn down, or off, your ability to burn fat. There is a longer downward spiral from years of this. But that was that post.

In this post, I want to look at exactly what you can do to turn yourself into a fat burning machine. This is not only about turning the fat burning on and creating a situation where you can drive a homeostasis for a steady and healthy weight, but is also about well-being and energy. My experience, as well as the overwhelming blogashpere and research itself, shows that an important benefit of fat adaptation is a much more stable energy level and well-being/mood.

We’ll look specifically at endurance athletes first. They want the same things that those who have problems with metabolic dysfunction want. They want to burn fat, not carbs, because humans have such a limited supply of carbs but much much bigger supplies of fat to draw upon. When athletes going long distances run out of carbs they are said “to hit the wall” or “bonk” (French for the noise your head makes when it hits the road?) So we’ll look at some of our lab results with an athlete later.

It’s not about treating carbs as evil and trying to run your body without carbs. In some ways it’s the exact opposite – it’s about sparing the glucose you do have. It’s about getting your body to do what it is designed to do under usual evolutionary conditions – burn fat and have enough energy to move all day and/or make short intense bursts. Becoming an efficient fat burner allows you to do just this.

Carb burners v Fat burners

If your metabolism is set up to predominately burn carbs, then you’ll most likely have many more highs and lows throughout the day energy wise. I call the lows “falling off the glucose cliff”. That’s when your glucose dependent brain cries out for more fuel – in the form of simple carbs usually. The cycle continues. If that’s you, then this blog could change your life for the better!

There are many plausible or proven health benefits here to. There is the obvious one of easily being able to control your weight. But far beyond that is reducing the damage high sugar, and high insulin, and sugar burning (glycolysis) do in your body. All of these are inflammatory and cause oxidative stress. These are the causative mechanisms behind chronic disease development including heart disease and stroke, diabetes, cancer, and brain (dys)function.

Fat burning in endurance exercise

One lab-based method we use to measure fat burning vs carb burning is the respiratory exchange ration (RER), also known as the respiratory quotient. This is the ratio between the amount of carbon dioxide exhaled and oxygen inhaled, which provides an indication of which substrate (fat, carbohydrate or a mix) is being used for fuel. We do this using our breath by breath gas analysis system in our Metabolic and Exercise Science Clinic at the Human Potential Centre at AUT Millennium Campus.

The RER varies between 0.7 (100% fat burning) through to ≥1.0 (100% Carb burning). A ratio of 0.85 has been labelled the metabolic efficiency point, when the body burns half of each. We try to determine what exercise output can be maintained for half and half. Bear in mind that everyone will eventually burn 100% carbs if the exercise is intense enough, but the higher the intensity at which fat is still the predominant energy source the better. However, what we are most concerned with is the ability to burn fat at rest and at lower to moderate intensities of exercise. This is great for weight loss. It’s great for health. But it’s also great if you are an athlete trying to do longer distance events like the Ironman triathlon.

We recently had a high level triathlete in our lab. We measured his RER before and after a 10 week training block going into this year’s Ironman NZ. We also transferred him to a low carb high fat (LCHF) diet for the period of that training. He was training about 20 hours a week and came in to the 10 week block relatively fit, albeit slightly heavier than he wished.

Some stats:

  1. Start weight 86 kg, post weight 78 kg. Good weight loss while reporting eating until full. No deprivation of food or calories if needed. Reduced calorie consumption on long training sessions. Few if any gels or sports drinks.
  2. Pre RER @ 270 W bike = 0.93, post RER @300 W = 0.82. This translates to a change in fat utilization from 23% of fuel to 60% of fuel at the same power output, for a lighter overall weight (power per kilo was also increased).
  3. Metabolic efficiency point (50/50 fuel use) improved from 180 W to 300 W. This shows the massive increase in efficiency we saw with a switch to a LCHF diet.

If you know anything about endurance training and racing then you’ll know that these results are outstanding. To the point of being spectacular. The limiting factor in longer races is not maximal output, but how fast you can go while conserving muscle and liver glycogen (carbs). You need to maximize your fat burning and preserve your very limited supply of carbs as much as possible.

Most athletes try to get around this problem by eating extra carbs during training and racing. This can work to an extent, but perversely raises insulin and shuts down your body’s ability to burn fat. It’s almost impossible to eat and digest enough carbohydrate to actually race these events well. You need a good degree of fat burning.

Anyway, this illustrates what can be achieved with a LCHF diet; good, effortless weight loss and spectacular performance gains.

If you’re not an athlete, and I’m assuming most of you are not, then the same principles still apply. We can hook you up to the gas analysis system and determine your “metabolic efficiency” at rest. We can assess just how much of a carb burner you are and we can track your progress if you decide to become a fat burning machine through a LCHF diet.

Fat adaptation v ketosis

There’s a special type of low carbohydrate diet called a ketotic diet. I want to explore that in the next post. Stay tuned.


Thanks to Helen Kilding for her help with this blog