The Science of Human Potential

Humans ferment fiber into fat

A short post on how fermentation of resistant starches in the gut into short chain fatty acids (SCFA) works and the role it plays in human and other animals’ diets.

I direct you all to a really nice review paper in the journal “Physiology Reviews” for way more expert and in-depth analysis than I can do. You better have some good biochemistry if you want to understand that paper though. Frankly, I was struggling by the end.

I am writing this because I have had a problem reconciling why mammals can have such varied diets yet end up running pretty similar organs and homeostatic biological systems. Even within humans, at least in the non-industrial food environment, we can flourish on such a wide range of macronutrients.

At one end of the animal kingdom we have herbivores, such as cows and gorillas, eating plant only diets. At the other end we have carnivorous cats of various sorts, like tigers and lions, eating meat. One end appears to be a low fat, high carb, moderate protein diet. The other is a high fat, high protein diet.

Humans are the same. We have Inuits at one end on a high fat, virtually no carb, moderate to high protein diet. At the other end we have the Kitavans in Papua New Guinea who eat high carbohydrate diets (have a look at Dr Staffan Lindberg’s site on this – it’s quite interesting). Yet both groups and all of the ones in between in their natural food environment are metabolically healthy and free of chronic disease. The same is true for the animals as well. All have no trouble maintaining a healthy weight even in the presence of plentiful food.

So what goes? And why do I talk about a low carbohydrate diet in the midst of all this evidence?

My short answer is that a whole food diet is fine in any macro-nutrient composition as long as you are metabolically healthy. But as soon as you become dysregulated (aka insulin resistant) – probably because of sugar and other lifestyle factors, like excess stress – then carbohydrate restriction is the way back out of this. This is probably half the western population, maybe more.

Why? Well the longer answer is that there is something else to consider in the animal and human digestive systems which further helps us (or me at least, and hopefully you too) reconcile the variation in carbs/fat/protein across animals and humans.

The emerging evidence it seems is that plant fiber is fermented in the gut of herbivores and omnivores, including humans. This provides energy in the form of short chain fatty acids, especially butyrate.

This is really cool because it means that the range of macro-nutrients which makes it through the gut into the actual bloodstream of all these very different, but similar, animals is similar. It’s much higher in fat than we previously thought. For example, studies with Western lowland gorillas shows that the majority of their energy (57%) comes from the SCFA fermented in the gut from vegetable fiber (SCFA are saturated fats!). Most of the animals we are considering, including humans, are on high fat, moderate protein, lower carb diets – give or take – once we take into account fiber fermentation in the (healthy) gut.

“The macronutrient profile of this diet would be as follows: 2.5% energy as fat, 24.3% protein, 15.8% available carbohydrate, with potentially 57.3% of metabolizable energy from short-chain fatty acids (SCFA) derived from colonic fermentation of fiber. Gorillas would therefore obtain considerable energy through fiber fermentation.”

Where things go astray is when any of these animals, including humans, eats processed carbohydrates. These aren’t high in fiber of course and go straight into the bloodstream. Insulin is constantly high in an attempt to move the carbs and it’s downhill from there.

Other researchers might have known about this for a long time, but I was sticking to the old “roughage hypothesis” of fiber digestion. That is, the idea that the fibre wasn’t digestible and helps clean out and stimulate the colon.

So what of humans then? I think we can take a few things away:

  1. Fermentation of fibre, like in herbivores, occurs in the human colon
  2. Much of this turns into usable SCFAs. Some feeds the actual bacteria, some the gut wall and some goes into the bloodstream and is processed from there.
  3. The calorie count on products which contain fiber is flawed, and another reason why a calorie is not a calorie. Celery is a good example of this; people claim celery contains less energy than it takes to digest – true enough, immediately available carbs are low, but the fiber fermented into fat contains significant amounts of calories in SCFAs.
  4. High carb diets which are high in fiber can turn into higher fat diets, and that is likely what has been the case historically for humans.
  5. Microbiome health is likely to depend on establishing quantities of bacteria which can digest fiber. This will depend on the history of feeding that sort of food. Processed carbs probably undermine the development of the gut bacteria needed to digest fiber.
  6. And processed carbs bypass the entire mechanism and dump insulin raising carbs into the system further upstream from the stomach and small intestine.

Reporting back on fat adaptation and making weight for triathlon

Unknown

Here’s a nice report back from a (kiwi) triathlete living in the Middle East who has become fat adapted and losing some weight in anticipation of the world champs in a couple of months. I think I talked her into a “trial” period of the LCHF, whole foods approach. This is her report after a few weeks.

Hey Grant,

Things are going well –we are well into week 3 .. or maybe it’s week 4…and don’t really see the need to “come off” adaptation phase… although close to giving into my on-going craving for whole grain buttered toast with manuka honey!

GS: JUst eat the damn bread and honey and you will probably feel a little bloated and decide that the thought was better than the actual real thing! Also carbs aren’t that dangerous….you did need to seriously restrict them to adapt though.

I’m enjoying the benefits of no slump in the afternoons.
I’ve become sick of eggs and have moved to a smoothie for breakfast and lunch –
Am really starting to cram everything possible into them! Loving it. Complete meal in a glass – yum –  see pic of regular ingredients.

Unknown-2

We are going through peanut butter like nothing else! So I have started making our own – success!! Who’d have known!? So easy!!! Tip salted or dry roasted nuts in a blitzer and 3 minutes later…. Delicious sugar-free and palm oil-free peanut butter 🙂

I am quite happy to continue – we have pretty much removed all sugar…. In-fact I had a fruit salad the other night and felt both very naughty and high from the sugar! In addition to my craving for toast with honey (… seems like a cardinal sin) I’m tempted by a few dates or prunes that are hidden in the naughty cupboard…… But I figure if these are my only “slips” I’m not doing too bad.

I’m consistently under 60-61kg now and nudging <60kg . Almost goal race weight.

One thing I found interesting over the weekend’s more testing session – the chomps that I was having about 50 mins and 1hour 30 mins into the session were really noticeable. I really felt the boost and as a result think I had a better training. Basically it was 90 mins of max accelerations (3 x pyramid from 10 sec to 60 sec) on the turbo and then 40 mins run off the bike including 15 x 30sec on-off efforts. Last weekend on the bike I really struggled and found it soul destroying trying to accelerate / hold max speed for 60secs and unable to hold max speed for long. This weekend I did much better and only towards the last 5-10 seconds did I loose power and the speed started to drop. I really think the new diet helped with endurance and enabled the carbs /fuel to really do their job 🙂

So things are going well and over-all Tim and I are noticing that we are eating a lot healthier and a lot less in each meal – get full earlier. I’m on the hunt for new recipes –bored of eggs ! and want to mix up dinners a bit. I think we run the risk of becoming smoothie junkies! They are so easy and satisfying! Will try lettuce leaf tacos this week and some sort of quiche or egg tart / pie…..

Anyways –feeling good and happy about the diet! Really glad we made the switch.

Cheers
Bex

I think she’s doing pretty well. My advice is really around using carbs in training when the demands of her training session warrant it. I’d still prefer the majority of training wasn’t in the mid-chronic cardio zone.  But if she is going there, then take the carbs you will need them.

Otherwise, mission accomplished so far, which was learning about how to be come fat adapted, eating whole foods, making a race weight and maintaining even energy.

Unknown-1

Schofield’s hormetic theory of wellbeing

photo[1]

My first whiteboard attempt at my hormetic theory of wellbeing

I had a few things click into place in the last week or two, around how to conceptualize and manage our well-being, especially considering all the biology involved.

Without being grandiose and egotistically naming a theory after myself, I think what I have come up with has some novel concepts. I do acknowledge the inspiration from a scientific paper, which lays out the (some) diet and exercise components of the hormesis of wellbeing (see here).

So here’s a summary of the theory (or at least the bringing together of a few different ideas):

  1. Hormesis is the adaptation to a stimulus which in a bigger dose is toxic. This stress exposure is central to, and even essential for, wellbeing.
  2. Hormetic stressors come form all sorts of things; including sun exposure and our food environments (eg, fasting).
  3. Wellbeing depends on a constant ability to have neuroplasticity (rewiring of the brain). Certain biological conditions must be present for  this to occur.
  4. These conditions include high levels of BDNF (brain derived neurotropic growth factor), low insulin, increased IGF-1, and low reactive oxygen specs (ROS).
  5. Hormesis drives these conditions in a similar way across a range of different stressors – too much or too little does exactly the opposite, more or less.

It’s a cool theory I think because it offers some simplicity and parsimony when thinking about the biology of wellbeing and what drives it.

So that’s it in a nutshell and here’s a bit more detail:

What is hormesis?

Hormesis is a theoretical phenomenon of dose-response relationships in which something (as a heavy metal or ionizing radiation) that produces harmful biological effects at moderate to high doses may produce beneficial effects at low doses.

In other words, it’s the theory of general adaptation and super compensation applied across a range of stimuli. Obviously the amount of the stimulus any biological organism can take depends upon its current state (genes plus recent exposures), but also the other stimuli that organism is experiencing. The stress from the different stimuli is likely to stress that same system concurrently (important for later).

Humans need to be exposed to hormetic stimuli to maintain biological function.  With no stress, the system adapts backwards as well. If you lie in bed for weeks, or travel into space with zero gravity, your body adapts just as fast as to no stress.

Bottom line: Hormesis is adaptation to mild stress.  Stress is not just good but essential to human health and wellbeing.

Can we define wellbeing biologically?

Here’s the next important step.  The human nervous system is a complex distributed neural network. It isn’t confined to the head – its throughout your body.  Mind-brain-body=same thing.  There are around 100 billion neurons in every human. Each can synapse to up to 7000 other neurons.  Because the hardware and the software are the same thing, you must constantly rewire the system to learn anything, to experience anything and remember it, to solve problems, to experience a worthwhile life. This happens at all ages.

We call this neuroplasticity.

How does this rewiring happen? We need to produce some key biological conditions.  This is centered around production of Brain-derived Neurotropic Growth Factor (BDNF). BDNF is the protein which stimulates this rewiring.

I’m arguing that the conditions which support BDNF production are central to wellbeing.

You guessed it. Hormesis drives BNDF production.

How hormesis drives wellbeing

In the figure below, I have tried to simplify the basic logic behind a hormetic response driving neuroplasticity. What is involved (simply) to optimize the biology of rewiring is low insulin, higher insulin-like growth factor 1 (IGF-1), and absence of reactive oxygen species (ROS).

What is interesting is that a range of hormetic stimuli, sometimes through different mechanisms, achieve the same biochemistry The opposite is true when we expose ourselves to too much of the same stimulus.  Once the stress response is maladaptive rather than hormetic, we produce insulin resistance, inflammation through ROS, and (sometimes) adverse levels of IGF-1 (see Figure below).

These ROS, insulin and IGF-1 do not always perfectly covary AND importantly they are also essential for humans one way or another for living.  We need insulin, we need ROS, we need flexibility in IGF-1 production. It’s just that the systeM needs to have metabolic flexibility to respond and rebuild (especially the nervous system).

Bottom line: Neuroplasticity is essential for human wellbeing and the supporting biology may be the center of the mechanism for feeling good. There is no evidence that hormesis drives this biology.

Hormesis.001

Specific hormesis

So I’ve tried to put together a start to the broader framework of understanding how various exposures to environmental stressors are highly beneficial to us in hormetic (adaptable) doses and directly drive the BDNF and neuroplasticity mechanism and therefore well-being.

These are known mechanisms in the basic research.

Exercise is a great example of hormesis in action.  This paper ” Impact of exercise on neuroplasticity-related proteins in spinal cord injured humans” showed a five-fold increase in BDNF in athletes after a 10 minute easy stint, but a decrease in BDNF after a marathon (42 km) event.

So exercise which we can easily accommodate and then adapt to drives the physiology of neuroplasticity and wellbeing. This is the hormetic response.  The stimulus (exercise) eventually becomes toxic at high and more intense doses.

So my theory is that there is a straight biological and hormetic connection to wellbeing through neuroplasticity for several (and there are likely more than I have identified here) important health and lifestyle behaviors.

I’ll get to the indirect effect later in this piece.

Some factors, like psychological stress, simply drive adrenal axis responses which would be appropriate for an acute “fight or flight” short lifesaving sprint, but are entirely inappropriate and toxic applied chronically. Chronic psychological stress is known to drive reduced insulin sensitivity and increased ROS.

Others, like exercise, offers a balance. You need the stress, but too much is toxic.  Sunlight exposure is like this.  Some exposure drives Vitamin D production.  There is good evidence to show the antioxidant (ROS defeating) effects of Vitamin D, as well as the vascular effects and increased insulin sensitivity through nitrate availability, but if you go and get sunburned then you will see the opposite effect.

Food is a really interesting stimulus. I think what we want is both the hormetic effect of the occasional fast, which is known to promote a catabolic (repair) effect and reduce ROS, IGF-1 increases, and low insulin. Obviously fasting for too long might have the opposite effect through probably high cortisol production. Equally, we need the anabolic effect of eating and the nutrients supplied by food. Too much food, especially junk processed carbs, bangs up insulin and ROS. So I think the intermittent fasting people are onto something when they cycle in and out of food availability.

Metabolic flexibility is an overriding theme here too.

By that I think that when you become metabolically dysfunctional and are constantly hyperinsulinemic and have high ROS, you really have the least effective system for neuroplasticity and cognitive rewiring.

Another factor is the health of your gut microbiome.  Again, when not in its usual human supporting and symbiotic form, this is inflammatory.  It helps create insulin resistance, ROS everywhere, and general metabolic dysfunction.

You’ll see below several ideas and mechanisms I propose. If you think of more then let me know.

Actually I just thought of another – brief ice baths.  Short exposure-reduced ROS and increased insulin sensitivity.  Too long=severe stress and probably increased ROS?

Hormesis 1.002 Hormesis 2.003

Indirect effects and wellbeing

Where positive psychology fits in here is something I have been thinking carefully about.  I, along with others, have been into that field for a while now and we talk about creating social networks, being nice to others, giving your time and resources to others, and many other things. Have a look at our Sovereign NZ wellbeing index for the full meal deal.

So indeed these are important, but because many create the resources you need to buffer stress and control the exposure to the potentially toxic stimuli. Having a social network for example means you will less easily be overwhelmed by stress and more in control of your life.

A more distant indirect effect is money.  Money by itself clearly has no direct effect on your BDNF, insulin, ROS and so forth. I’m pretty sure no one has done this study, but I predict that sitting and staring at a large pile of cash has very little effect on these!

But money gives you the resources.  The time and space to create the networks, to give to others, and to control the exposures to the life stresses you want and thrive on.

Bottom line: Hormetic stress is the biological basis of wellbeing.  We see good evidence across a range of environmental stressors how this all works. This brings the “Primal” type approach right into mainstream science where it belongs.  I know the primal/paleo guys have been saying this for years, but we do need to convincingly bring the biology and the practice together which is what I’m trying to do.

Finally….

This is a theory of stress, but in a controlled and balanced way.

I am critical of much of the work in public health, quite a bit of which I have done myself.  We often try to understand how a single factor (e.g., exercise) is related to wellbeing. We assume a linear model where more is better and the dose applies across the population.

Clearly, in this hormetic, model that is just rubbish.  Everyone can take a different amount of a particular stress (say exercise).  What they can take and probably adapt to (hormesis) depends on:

  • Their genes
  • Their exposure to exercise in their lifetime, weighted more heavily recently
  • The sum of all the other stressors they are currently being exposed to – obviously there’s less chance of adapting to an exercise session if you are sunburned and had a poor night’s sleep and an argument with your wife.

So what this all means is that what you need to optimize your potential at anytime is highly dynamic and different for you now than it was yesterday.  And you almost certainly won’t resemble the same profile as others around you.

Last bottom line…

Moderation and stress that you can adapt to is crucial for well-being.

My dog won’t eat Big Macs – what should I feed him?

photo

Bluey sniffs out a half rabbit this morning

My dog eats pretty much anything, except three things which he doesn’t regard as food. These are – Big Macs, his own crap, and some commercial dog foods.  Other than that he’s good to go.

But what should dogs eat if you are trying to apply a paleo/primal philosophy to your whole family, including the dog?

I’m onto my third border collie, Bluey.  I love running and playing and generally having him as part of the family.  Our family eats whole food with a paleo philosophy where possible.  That considered, what should Bluey eat?  He’s a dog, not a human, and humans and dogs (probably they were actually wolves then) came together around the time of the agricultural (see a study on this)  revolution.  There have been many more generations of dogs than humans over that time.  They have had to change with us alongside us selectively breeding the ones we wanted.

There is evidence that they are adapted to digest starches better than their wolf cousins (see study In Nature).  In fact, there is no such thing as a “paleo” perspective for a dog because they weren’t around in their current form. My take is that modern dogs are in human symbiosis.

So I’ve been thinking a lot about what would be a healthy diet for Bluey.

Here’s what I have come up with – along with some principles.

Commercial pet food?

I am assuming that because there is no law in most countries (including NZ) that requires manufactures of pet food to have actual nutritional composition on their food, that this means that the food is probably relatively low quality. Nutrient density is likely to be poor, and how animals do on these sorts of foods is unlikely to be explored.

My bottom line assumption is that there is no sensible business reason for pet food manufacturers to make high quality food.  Even the premium brands; we have no way of knowing what is actually in them and if animals do well on them.

Should we ask veterinarians what they think on the issue? Probably not…they have a serious conflict of interest. It’s such a hard business to make money as a vet.  No government subsidies.  Pet food is a big earner and they survive by selling you this stuff. I’m assuming most vets do actually like animals and want to see them do well, but they really have no training in the science of nutrition (although to be fair that training in human nutrition appears to have been a disadvantage in modern medicine).

Bottom line: Modern commercial pet food is almost certainly poor quality and scarce of nutrients.  There is no sensible commercial reason to make it high quality. Avoid it.

ps, if someone can show me some “nutrient dense” commercial food then cool.

Are dogs carnivores?

Nope, they can eat starches and other veges. They can eat raw meats and be quite happy. The have a mouth structure which is full of canines, some molars (I can feel a couple at the very back of Bluey’s mouth) and some small incisors at the front.  I am assuming that are evolved to chomp up things tother than meat and bones.

So what is Bluey eating?

  • Whole rabbit – shot on Great Barrier Island and bought from Canivoro in Akotaganga Drive, Northcote  (who I don’t get free stuff from and have no financial interest in). I’m assuming that a whole wild animal eaten raw with bones and organs has some decent nutritional value for a dog.
  • Some dried food – we are using the last of it. I agree its crap but I’m too tight to throw it out!
  • Goat, beef, horse – again from Carnivoro – same as above; at least likely to have some nutritional density.
  • Bones – lamb shanks, pork ribs, chicken carcasses etc – Our family eats all these meats and what we don’t eat we give to Bluey.  I am assuming that scavenging off humans for bones is likely to be a “evolutionary heritage” for modern dog?
  • Left overs –  bacon, eggs and other scraps the kids throw to him and various left overs on bowls that he displays some interest in. Frankly, this is simply laziness as it helps us do the dishes (the first stage of it anyway) and produces less waste. We do wash the plates properly after Bluey’s done his bit I promise!
  • Crap – from any other animal including humans (some claim this is the reason they became endeared to humans in the first place!). I don’t willingly feed this to him as it grosses me out, especially when he later licks me….but he finds shit around the place from time to time.

What he doesn’t eat

The only things he has sniffed and walked away from are:

  • a Big Mac
  • Several varieties of commercial dog food. I guess he didn’t regard that as food!
  • His own crap

Can you have a vegan dog?

Apparently there are such animals living quite well and actually having quite long lives. Who knows how or why? Perhaps they do have such metabolic efficiency.  Perhaps they are essentially on severe caloric restriction and therefore live longer like other calorie restricted animals do. Who knows?

I doubt any dog willingly chooses not to eat raw meat though!

Ditch on the Barrier

Getting some real dog food on Great Barrier Island

Saturated fat is bad for you…….really???

Unknown

by Grant Schofield and Helen Kilding

Addendum note from Grant: This post has generated an enormous amount of debate – see the comments section.  Its interesting as the authors of this study came back into the debate early.

Another study, this time it’s my colleagues much closer to home in New Zealand, and they received quite a bit of media space from it. The authors sought to estimate the potential impact on cardiovascular health of modifying dietary intake of saturated fat across the New Zealand population, and whether this would be appropriate and feasible.

They decided that while there was no evidence that fat intake affected health, substituting saturated fats with polyunsaturated fats would be of use and is “feasible” for the health of New Zealanders.

Here’s the paper. “Review of the evidence for the potential impact and feasibility of substituting saturated fat in the New Zealand diet (Rachel H. Foster, Nick Wilson, Burden of Disease, Epidemiology, Equity and Cost-Effectiveness (BODE3) Programme, Department of Public Health, University of Otago – Wellington, New Zealand).

They concluded that “Replacing 5% of daily energy consumed as saturated fat with polyunsaturated fats would be expected to reduce cardiovascular events by about 10%.”

Here’s what the media made of it – The New Zealand Herald, and Stuff.co.nz

And I got more than a few questions from readers….for example:

Hi Grant

What’s your take on this study? (see attached)

Many of the fats they mention as bad I have been eating for the past two months and have lost weight and improved cholesterol! This is an actual result and if anything by default resulted in me consuming less of their so called good fats i.e canola oils, polyunsaturated oils etc.

No wonder it  is hard for people to make informed decisions about diet with so much conflicting information. End of the day I decided to see for myself and make myself the test subject on a LCHF diet and continue to be thankful I did.

So what do we make of all this? First, they actually found no association between fat intake and disease outcomes in their meta-analysis. So great, fat isn’t a risk. But they did conclude that because replacing saturated fat reduces risk, that saturated fat must therefore be a risk factor.

I guess they haven’t considered the latest meta analysis in the American Journal of Public Health (2013)  “Food Sources of Saturated Fat and the Association With Mortality: A Meta-Analysis “. This specifically looks at saturated fats. They show very limited evidence for most saturated fats foods having any association with CVD or cancer. Probably processed meat is the strongest association. In this sort of food product, saturated fat isn’t the only metabolic ingredient.

Nor have they considered that actual experimental evidence through randomized controlled trials (there are more than 20 now) does not show a harm for increasing saturated fat intake in LCHF diets. All the “established” cardio-metabolic risk markers show very favorable outcomes compared with all other diets. No long term outcomes, but these are well known and regarded proxies.

The recently published Sydney Heart study data shows that exactly the opposite happened back in the 1970s, when they replaced saturated fat with polyunsaturated fat and saw things get worse. Here’s the BMJ editorial on this. And here are some results:

“Participants were randomly divided into two groups. The intervention group was instructed to reduce saturated fats (from animal fats, common margarines and shortenings) to less than 10% of energy intake and to increase linoleic acid (from safflower oil and safflower oil polyunsaturated margarine) to 15% of energy intake. Safflower oil is a concentrated source of omega-6 linoleic acid and provides no omega-3 PUFAs. The control group received no specific dietary advice.

Both groups had regular assessments and completed food diaries for an average of 39 months. All non-dietary aspects of the study were designed to be equal in both groups.

The results show that the omega-6 linoleic acid group had a higher risk of death from all causes, as well as from cardiovascular disease and coronary heart disease, compared with the control group.”

Nor have they considered almost all of the growing mechanistic evidence that metabolic issues, including CVD, are inflammatory based and the evidence points strongly to a myriad of interacting pathways, from gut microbiome, to sugar, to simple carbs, to the stress axis, to VLDL and triglycerides through the liver etc etc. The direct effect of dietary saturated fat is not clear in any of these mechanisms and unlikely to be a factor.

Overall, the evidence from the association studies is weak, equivocal, or inconsistent, depending on what term you like best.  Experimentally and mechanistically it doesn’t stack up.  Come on guys, are you doing your reading? It’s not good enough when there is such a broader amount of evidence. Your study doesn’t lead to a rationale for reducing saturated fat and replacing it with polyunsaturated.

Worse still, you’re promoting the use of manufactured vegetables oils which are high in Omega 6 and likely to be inflammatory, adding further to the problem.  These oils are also quite unstable and easily oxidized further, adding to metabolic problems. Saturated fat is not.

Avoiding fat will likely mean eating more carbohydrate.  For many, this will further dysregulate their carbohydrate metabolism and make them more insulin resistant resulting in a downward cycle with all the direct and indirect effects of hyoerinsulinemia.  These guys just haven’t even thought that the active metabolic ingredient in their weak epidemiology might be something else which they haven’t or can’t control for…..insulin-raising carbs.

WHAT I THINK WE SHOULD THINK ABOUT WITH FAT:

  1. Fat contains loads of calories
  2. Fat is an essential nutrient
  3. Highly processed fats are inflammatory
  4. Good quality whole foods, including loads of vegetables, are good for you.  Their fat content appears not to harm you.
  5. Omega 3 fats are good for you. These are poly unsaturated so if that is what they are talking about then great.  But these guys go on to talk specifically about manufactured seed oils – these are not good.
  6. In high carb, insulin-provoking diets, fat seems to add to the insulin response.  This seems to be worse in people who are insulin resistant.  By itself, fat is metabolically benign, at least as far as insulin response is concerned. A good reason to avoid the standard American diet.
  7. Processed meats are likely to be bad for you.  I’m not sure if it’s the actual fat and I’m not sure what the mechanisms might be – inflammatory? We may never know if they are for sure because no one is likely to run an experimental trial where people get a long dose of processed meat.

Take home messages:

  • Don’t believe everything you see in a scientific paper.  Sometimes they go past the evidence.
  • Carry on eating fat, hopefully in the absence of processed and simple carbs as they may harm you in combination.

How did fat get such a bad name in the first place?

We’ve been brainwashed in to thinking that when we eat saturated fat it goes straight into our bloodstream, instantly bonding to the inside of our arteries, eventually clogging them up completely. This is bullshit. Atherosclerosis is caused by oxidised LDL particles penetrating our arterial walls, inciting inflammation and damaging the arterial tissue. And what increases LDL particle number?

  1. Insulin resistance and metabolic syndrome
  2. Poor thyroid function
  3. Infections
  4. Leaky gut
  5. Genetics

Let’s look at that list again…..no mention of dietary intake of saturated fat.

And when we talk about saturated fat, everyone always wants to talk about cholesterol. Dietary cholesterol does not affect total blood cholesterol. In fact, when we do eat cholesterol, our body makes less of it to keep our blood levels in balance.

So even if eating fat doesn’t result in CVD, won’t eating fat make us fat?

No again. As we’ve said before, fat doesn’t make you fat. Fat is very satisfying, especially when paired with low-carb eating. A nice steak rippled with fat is far more filling than some crusty bread spread with butter. You’ll eat a decent piece of the former and be satisfied but could easily polish off half a loaf of the bread with a good helping of butter and still be hungry. It’s difficult to overeat on a high-fat, low-carb diet.

Our bodies want to use fat for energy, but when we eat fat in the presence of large amounts of dietary carbohydrates, it makes it difficult to access fat for energy. On the flip side, dietary fat in the presence of low levels of dietary carbohydrates makes it easier to access fat for energy. It’s also easy to overeat fat and carbs together – think hot chips, buttered toast, milk chocolate.

And let’s think about farming for a second….how do you fatten cattle? You feed them lots of lots of grass (a carbohydrate). According to a recent post on Christine Cronau’s Facebook page, “70 years ago, farmers tried to fatten their livestock with saturated fat. It backfired! The pigs lost weight and became more active. Of course, the farmers weren’t silly enough to persist with something that didn’t work, yet our conventional health professionals have insisted on doing so!” I’ve tried to source more detail on this but have drawn a blank so far.

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.

Does carb burning age you?

6a00d8341c368353ef00e54f6c1d8b8834-500wi

Grant was out for his weekly hill ride with his old mate Stephen. Stephen was now in his nineties and Grant just about to turn 90. The day was sunny and warm. At halfway, they stopped and had a coffee and talked about their grandchildren, each showing off a bit to the other. On the last high hill Grant took off and lead out a sprint. It was all good until just as they hit the top, Grant felt a sudden pain in his chest and dropped dead. Stephen, after a lifetime of never quite winning the hill sprints, seeing him falter took his chance and rode past him – at the exact moment he finally won a sprint, he too felt a sudden pain and dropped dead.

Neither man even had the chance to pull over and unclip from their carbon racing bikes. They lay turtle up, each having won the final sprint to the line.

As Mark Sisson puts it, “they lived long and dropped dead”. Good quantity and great quality.

Anyway, that’s my little fantasy and thought experiment about how I should die along with my long time mate Stephen Farrell, who strangely thrashes me at everything except hill climbs.

Two things are inevitable in life, death and taxes.

I’m here to talk about the first one. I am assuming we want both quantity and quality of life. How do you get the most “bang for your buck” so to speak? The first clue might be in the caloric restriction data – eat less live longer. Sounds feasible, and some data support this idea. The unappealing thing, to me at least, is that eating is fun, enjoyable, and perhaps in the end the trade off isn’t worth it because you are alive but had to go hungry the whole time so life was just way less fun. But there are new data and new hypotheses about how glucose metabolism may be the driver, not caloric restriction.

How glucose metabolism fits in

I want to spend the main part of this blog summarizing (at least as well I can summarize a complex neurophysiology paper) how glucose metabolism controls the aging process, mainly through the brain. I’m talking about a paper just published in Trends in Endocrinlogy and Metabolism called “Metabolic mystery: aging, obesity, diabetes, and the ventromedial hypothalamus” available here. First, its hardly light bedtime reading, unless you quickly want to fall asleep. Second, there is so much complex genetics, animal study material, and hormonal and neuronal mechanistic stuff it takes a very long time to get through it. So I’ll spare you all the challenge and get straight to the major hypotheses and practical implications.

They start by revisiting the well known phenomenon that caloric restriction can increase lifespan, in at least some animals. Possibly humans and primates, although the jury is still out on that, and the only decent primate study wasn’t a decent study after all because of the high sugar diets for both caloric restriction and ad lib feeding groups.

Major findings of this review

  1. The energy mediating centre in the brain (the ventromedial hypothalamus) has specific glucose and FFA (free fatty acid) sensors.
  2. These sensors directly affect hepatic (liver) and peripheral (muscle and organ) glucose metabolism in opposite ways.
  3. High glucose in the blood drives a decrease in liver glucose production and an increase in glucose metabolism in other tissues. It’s vice versa for lower glucose and increased FFAs in the blood.
  4. Increased oxidation of glucose in peripheral tissues requires less oxygen to metabolise but results in more oxidative stress (i.e. damage) to the tissues. This damage is directly implicated in aging. Increased availability of insulin and insulin-like growth factor 1 (IGF-1) are also implicated in this process.
  5. Glucose on its own may not be enough. Increased mortality of Type 2 diabetics who are aggressively treated with exogenous insulin is evidence for this.
  6. Take home message – there is direct evidence that high dietary glucose load (read CARBOHYDRATE) Read More

How happy are New Zealanders?

SWI

How happy are you?  How well are you doing in your life?  How happy are New Zealanders, and how do they compare with other countries?

All big questions. You can find out how you compare with the average New Zealander of your age and sex here.  You can access the Sovereign New Zealand Wellbeing Index here.  You can view TVNZ’s Sunday episode aired on the topic here.

I am very proud to announce the public release of this Sovereign New Zealand Wellbeing Index. It’s the first survey point in a six-year research partnership with Sovereign .  It’s also the first time anyone has tried to understand the epidemiology of wellbeing in a large (n=10,000) population representative sample in NZ.  We will follow some of the same cohort across the six years. The basic logic is that if you want to improve the wellbeing of the population, then first you had better measure it, and generate some hypothesis forming associations.

We also used the same measures as used in the European Social Survey wellbeing module.

So this has been several months’ work for me, and even more work for my dedicated research team, as well as a team at Sovereign working on the comms side.  Thanks everyone for the enormous amount of work.

Actually, that’s been the coolest thing about this project. The well developed comms and advocacy angle that Sovereign has been able to bring to the partnership.  They’ve got an interest in reducing stress and increasing wellbeing straight out form a claims perspective as well as the corporate social responsibility angle

Frankly, we are very used to doing high quality research which mostly gets published in journals a few people read, and a few masters and PhD theses which even fewer (maybe even only a few!) people read.

So now, we have had a great link into releasing the report, advocating government and policy makers, getting TV and media coverage of the results and so forth.

Mostly, I’ve been blogging about nutrition, exercise, weight loss and chronic disease prevention and treatment research at the Human Potential Centre at AUT University. That’s where I am a Professor (Public Health) and the Director of this research centre.  I will do a few more blogs in the wellbeing space to augment this report release.

Wellbeing is an area we are really getting into.  We are trying to bring many of the principles of positive psychology into health. We also want to bring some of the principles of health, especially nutrition and exercise into positive psychology. Each discipline has lots to offer, but combined even more so.

These sorts of national accounts or indices of wellbeing have become popular in Europe recently and other less robust world-wide measures like the Happy Planet Index. To our knowledge, we are the first to do both mainstream health measures and wellbeing measures.

Sunday on TVNZ did a great job of presenting some of the results.  Thanks TVNZ.  See here.

You can go online and either take the entire survey and see what we measured, or just the “7-item flourishing scale”   Goto www.mywellbeing.co.nz. We have the norms for your age and sex, so you can compare you results with those overall and of similar kiwis in the survey.  Have a go its fun.  Take the quiz.

Results for the Sovereign Wellbeing Index (This is the exec summary – get the full report here)

This report presents key findings from the Sovereign Wellbeing Index about the wellbeing of New Zealand adults in late 2012. The survey is the first national representation of how New Zealanders are faring on a personal and social level. The Sovereign Wellbeing Index provides a much needed look into how New Zealanders are coping within the economic conditions.

Wellbeing around New Zealand

Using flourishing as a measure of wellbeing there were small but consistent effects of gender, age and income. Older, female and wealthier New Zealanders on average showed higher flourishing scores. Similar findings were found across all other measures of wellbeing giving some confidence in the convergence of measures.

  • There were only small differences in average flourishing scores between ethnic groups (NZ European slightly higher than Asian) and regions across New Zealand.
  • Social position was a powerful indicator of wellbeing. Those higher on the social ladder reported much higher wellbeing.
  • The five Winning Ways to Wellbeing were all strongly associated with higher wellbeing. People who socially connected with others (Connect), gave time and resources to others (Give), were able to appreciate and take notice of things around them (Take notice), were learning new things in their life (Keep learning), and were physically active (Be Active) experienced higher levels of wellbeing.

Super Wellbeing

We looked at the 25% of the population with the highest wellbeing scores and examined what factors defined this group from the rest of the population. This underpins the idea that psychological wealth and resources can be identified and public policy and action, and personal resources utilised to improve these determinants.

  1. Similar findings to wellbeing in general were identified. Females were 1.4 times more likely to be in the super wellbeing group than males. More older, higher income, and higher social position New Zealanders were in the super wellbeing group.
  2. Connecting, Giving, Taking notice, Keeping learning, and Being active were all strongly associated with super wellbeing.
  3. Other health measures were also strongly associated with super wellbeing. These included better overall general health, non-smokers, exercisers and those with healthier diets and weights were all more likely to experience super wellbeing.

International comparisons

When compared with 22 European countries using the same population measures, New Zealand consistently ranks near the bottom of the ranking in both Personal and Social Wellbeing. New Zealand is well behind the Scandinavian countries that lead these measures.

New Zealand ranks 17th in Personal Wellbeing. Personal Wellbeing is made up of the measures of Emotional Wellbeing (rank 16th), Satisfying Life (rank 16th), Vitality (rank 16th), Resilience and Self- esteem (rank 19th), and Positive Functioning (rank 23rd).

New Zealanders did however rank above the mean for happiness, absence of negative feelings and enjoyment of life. However, we were still well below the top ranked countries.

New Zealand ranks 22nd in Social Wellbeing. Social Wellbeing is made up of the dimensions of Supportive Relations (rank 21st), Felt lonely (rank 20th), Meet socially (rank 21st), Trust and Belonging (rank 23rd), People in local area help one another (rank 21st), Treated with respect (rank 22nd), Feel close to people in local area (rank 23rd), and most people can be trusted (rank 11th).

Further exploration of our worst-ranked Social Wellbeing indicator ‘Feeling close to people in local area’ showed considerable variation across the country with the major cities scoring worst with Auckland at the top. Regional areas fared somewhat better. Younger people and NZ European New Zealanders scored lowest.

Future

New Zealanders make choices everyday about their wellbeing. These are both personal choices as well as democratic choices about public policy and action at local and national levels. It is our vision that this index can help frame both personal choices and public policy and action in New Zealand. If it isn’t wellbeing for ourselves and others we are ultimately striving for, then what is it?

The Sovereign Wellbeing Index will continue to monitor the wellbeing of New Zealanders over the next four years. We plan to follow-up some of the participants in this nationally representative cohort to see how their wellbeing changes with time as well as continue to run this national index and benchmark indicators against European countries.

The cause of obesity – opportunistic voracity?

ObesityOK, here’s some real evidence of why the science of nutrition and metabolism is in such a mess. It’s an email discussion between myself and Professor Boyd Swinburn about the role of insulin and other metabolic factors in overweight and obesity, including weight loss.
It gets scientific and technical in places, but I think it’s an interesting debate to have. It’s also long (3000 words..).
The reality is, we both (Boyd and I) want the same thing – a healthier and happier population – but differences in our beliefs around the underlying causes of the problem make a big difference to how we approach the solutions.
Boyd argues that the reason we are so fat is because we are in a “hypercaloric environment”. There’s just too much food laying around, the exact type (carbs, fat etc) doesn’t matter. That drives “opportunistic voracity” (great words!). That means that there’s heaps of food around and we just gobble up too many calories. Metabolic partitioning and macronutrient intake has very little to do with it, although in Boyd’s words “the science of the particular dangers of saturated fat is long since settled”. He is not only adamant, but convincing and speaks strongly about exactly this.
His argument is a calorie is a calorie. My argument is that this isn’t the case at all. Human energy metabolism is controlled by hormones, specifically insulin and leptin as the main drivers. These are affected by several factors, a main one is dietary carbs.
Boyd is a highly accomplished academic in public heath obesity work. He also has a background in metabolism as you will see. He’s an MD and Professor of Population Nutrition and Global Health at the University of Auckland AND is the Alfred Deakin Professor, and Co-Director of the WHO Collaborating Centre for Obesity Prevention at Deakin University in Melbourne.
I also asked Prof Tim Noakes (Professor of Exercise and Sports Science at the University of Cape Town, and well known in the new nutrition paradigm) to have a read and see what he made of the debate.
It all started with a discussion on a flight to Rotorua about insulin and weight. Boyd pointed me to a couple of papers he authored in the 1990s where they looked at the metabolic state of weight gainers in Pima Indians. These were detailed metabolic studies. See this description of how the most insulin resistant Pima Indians gained the least weight (counter intuitive to what I would argue). The trouble is that the cross sectional and the (uncontrolled) longitudinal findings are completely opposite to each other.
At baseline, the most obese people tended to have high absolute resting metabolic rate, low RQ (high amount of fat oxidation), and insulin resistance. After 3 years, the ones who put on the most weight were the highest carb burners (higher RQ), had the lowest resting metabolic rate, and were the most insulin sensitive.
Note: RQ (Respiratory Quotient measures how much fat you burn for fuel v how much carbohydrate you burn. Low RQ=fat burner, high RQ=carb burner
So what do you make of all of this, and why should anyone care?
Well, it is a very important metabolic argument about what happens in the body to dysregulate your homeostasis of energy balance and cause weight gain. I say that the food we eat drives subsequent fat storage or fat burning. Hunger and fullness from food depends on the interaction between the carbs, fat, and protein in the food and the person eating it. High carbs means less satiation, more overeating and more fat storage; less carbs results in the opposite.
Anyway, if you like a bit of hardcore science, here’s the discussion Boyd (BS) and I (GS) had. It gives you a feel for how far apart obesity researchers actually are on very important topics – like what causes us to get fat.
Opportunistic voracity or hormonal energy homeostasis?

To: Boyd Swinburn

Subject: Re: papers

GS=Grant Schofield, BS=Boyd Swinburn, GS=Gnant second response

GS: The debate then in the discussion [of your Pima Indian paper] isn’t around the fact that RQ is modifiable by macronutrient composition, but that fat mass drives RQ?

BS: I THINK RQ IS AFFECTED BY MANY THINGS AND ACUTELY OF COURSE IT IS THE NUTRIENT LOAD AND NUTRIENT MIX. CHRONICALLY, AS I REMEMBER, IT IS MAINLY ENERGY BALANCE AND FAT MASS

GS: Given that industrial food [or Std American] diets are moderate carb at least, many who eat them are hyperinsulinemic most of the day. What I am arguing is that RQ is mostly to a point which turns off lypolysis, most of the time. Fasting insulin may be a different story, but less important because of the continual high insulin from carb ingestion. Sugar probably provides a mechanism to increase insulin resistance further.

GS: I maintain that eating sufficiently low dietary carbs and high fat reduces RQ.

BS: YES SURE

GS: LCHF is known to be more effective for weight loss maintenance in free living trials ad lib, than calorie restricted low fat diets.

BS: GENERALLY, ALL DIETS WORK TO REDUCE WEIGHT IF THE RULES OF THE DIET ARE ABLE TO BE FOLLOWED AND IF FOLLOWED ARE HYPOCALORIC. ALL DIETS ALSO SHOW THE SAME RETURN TO PREVIOUS WEIGHT (METABOLIC BRAKES ON WEIGHT LOSS PLUS RETURN TO THE OBESOGENIC ENVIRONMENT AND OLD HABITS). THE ONLY ‘METABOLIC’ EFFECT THAT I AM CONVINCED OF IS THE EFFECT OF PROTEIN ON SATIATION.

YOU HAVE TO BE CAREFUL ABOUT IMPLYING METABOLIC MECHANISMS FROM AN EDUCATIONAL INTERVENTION, I THINK. THE STUDY THAT WAS INFLUENTIAL FOR ME WAS THE KENDALL STUDY OF 11 WEEKS OF SURREPTITIOUS HIGH FAT V HIGH CHO.

KENDALL AM J CLIN NUTR 1991 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=2021123

GS: Here’s what these guys did and found “Thirteen females were randomly assigned to either a low-fat diet (20-25% of calories as fat) or a control diet (35-40% fat) for 11 weeks. After a 7-wk washout period, the conditions were reversed for another 11 weeks. Energy intake on the low-fat diet gradually increased by 0.092 kJ/wk, resulting in a total caloric compensation of 35% by the end of the 11-wk treatment period. This failure to compensate calorically on the low-fat diet resulted in a deficit of 1.22 kJ/d and a weight loss of 2.5 kg in 11 weeks, twice the amount of weight lost on the control diet. These results demonstrate that body weight can be lost merely by reducing the fat content of the diet without the need to voluntarily restrict food intake.”

Yes, caloric deficit and short term weight loss on a low fat diet is seen. Plenty of research on that. Yes, eventually most people return to previous weights, but this is in an environment which is overrun by dietary carbs and processed ones at that. The problem is over-exposure to food as you say it is the processed carbs that are the problem in the food though not the fat.

The Kendall paper pits a low fat diet against a moderate fat.moderate carb diet which is nothing to do with a LCHF diet.

Good points though about problems with diet and weight loss research. Educational lead programs – where we tell them what to do and some lose weight – is how much research is conducted. Of course, we don’t understand the metabolic effects of it clearly because people vary in their application and adherence. We could do more metabolic ward, respiratory chamber diet studies. We will never get the funding to do those in my country though, at least not through our Health Research Council, which funds a max of $1.2 million for a three year project, much of which is kept centrally by university administration as the salary overheads are 100%.

On the other hand, public health recommendations should be based on what people will do and find sustainable, so we do need to find the best weight loss and metabolic health programs people can actually follow. LCHF diets offer more promise than other regimes at this point. The 18+ RCTs to date show better weight loss, better cardio-metabolic parameter improvements, and better adherence wins in the short and medium term. I agree, long term outcomes are a problem for all diets, mostly because of the obesogenic environment. We all agree on that, but we don’t agree on what that actually is. I say it’s the processed carbs, you say its just food in general.

I’d also put forward a hypothesis that all diets work because they sufficiently lower serum insulin allowing lipolysis. You said I would lose weight on a hypocaloric high CHO/sugar diet in a previous conversation. Would I? I probably would as I am insulin sensitive. Would someone who isn’t?

GS: The hypothesis is that different macronutrient’s compositions have different metabolic effects, mainly through stimulating insulin more or less. Insulin directly affects RQ.

BS: INSULIN DOES ENORMOUSLY AFFECT RQ. MACRONUTRIENT COMPOSITION HAS A LOT OF DIFFERENTIAL METABOLIC EFFECTS ON LIPIDS AND HORMONES ETC. BUT FOR MACRONUTRIENT COMPOSITION TO AFFECT ENERGY BALANCE, IT NEEDS TO AFFECT EI OR EE – THE FACT THAT IT AFFECTS FFA FLUX, RQ ETC IS NOT GOOD ENOUGH. THERE ARE CLEAR MECHANISMS FOR HIGH FAT INCREASING EI THROUGH ENERGY DENSITY AND IT SLIPPING ‘UNDER THE ENERGY-BALANCE DETECTION RADAR’. ALSO, HIGH CHO DIETS FROM REAL FOODS ARE BULKY AND TEND TO REDUCE EI. IN ISOCALORIC STUDIES I DID IN METABOLIC WARDS IN OVERWEIGHT/OBESE PEOPLE, GETTING THEM TO FORCE DOWN ENOUGH FOOD ON A HIGH CHO (REAL FOOD, HIGH FIBRE) DIET TO KEEP THEM ISOCALORIC WAS HARD WORK.

GS: My understanding is that RQ has effects on lipolysis and fat storage. High RQ makes you store dietary carbs as fat and fat as fat if there is no high energy flux. All the research on the other clear mechanisms are in the context of a modern at least moderate carb diet. Using a LCHF approach, these mechanisms may not act the same way. In other words, when RQ is low because carbs are low you won’t store fat as easily, as the main mechanism isn’t activated. That’s the practical and experimental experience of people exposed to these (LCHF) regimes.

A couple of other points we discussed…

GS 1: Every low carb high fat trial [18 RCTs] shows favourable improvements in every CVD risk factor with big increases in saturated fat intake. That is not consistent with saturated fat being an important risk factor. There’s quite a bit published on this.

BS: IT HAS BEEN A WHILE SINCE I LOOKED AT ALL THIS STUFF. I UNDERSTAND THAT HIGH SIMPLE CHO HAS NEGATIVE EFFECTS ON TRIGLYCERIDES AND HDL AND THAT HIGH SAT FAT HAS A NEGATIVE EFFECT ON LDL. I BET THERE ARE A SERIOUS NUMBER OF META-ANALYSES OR POOLED ANALYSES ON THIS

GS: Yes the debate has moved on I think. All correct above, the fuller understanding of LDL particle size and number has increased our understanding of how this affects CVD risk. I’m not convinced that the saturated fat debate has done any public good and may have caused harm. There are prospective meta-analyses (see http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824152) and experimental studies showing the lack of evidence for saturated fat harm.

You will be aware of the main mechanism identified in CVD and other metabolic disorders. It’s chronic inflammation. I contend that hyperinsulinemia is inflammatory. A high CHO diet is therefore inflammatory.

GS 2: The assumption that every calorie has the same metabolic effect I think should be under scrutiny.

BS: I DON’T THINK ANYONE SAYS THAT MACRONUTRIENT COMPOSITION DOES NOT INFLUENCE METABOLISM (IN ITS BROAD SENSE). THE QUESTION NEEDS TO BE TIGHTER – IF YOU ARE TALKING ABOUT ENERGY BALANCE AS THE METABOLIC EFFECT, THEN YOU NEED TO DO SURREPTITIOUS ALTERATIONS TO REMOVE THE COGNITIVE/KNOWLEDGE EFFECTS.

GS: This sounds like you are saying we can only feed people either liquid bland meals, or meals identical in look and feel but with different macronutrient compositions, before you would take the results seriously. Surely we overcome almost all of your problems with eating actual food using RCT protocols or, in my experience, subjects as their own controls in ABAC. Or crossover designs? Your method lacks validity of being actual food, which of course is what humans usually eat. It’s not translatable into public policy or anything else really.

You should also really have a look at a more recent paper out of your previous NIH lab using the same Pima Indians and others. They show how carb burners eat more and gain more weight than fat burners. See here.

GS: Different macronutrients affect humans differently and the magnitude of effects varies depending on total meal composition and genetic and metabolic history.

BS: THIS IS A DIFFERENT QUESTION AGAIN – WITH EVERYTHING THAT AFFECTS A GROUP AS A WHOLE THERE IS HETEROGENEITY IN RESPONSE. THIS HETEROGENEITY INTERESTS SOME PEOPLE AND THOSE ARE THEIR RESEARCH QUESTIONS? THIS IS VERY DIFFERENT FROM THE AVERAGE AFFECT ON A GROUP OR POPULATION

GS: We should be interested in how the responders and non-responders differ in experimental trials. After all, some people stay healthy metabolically on an industrial food diet and others suffer. What is it about those who suffer? That’s where the term carbohydrate intolerance came from and we should take that term and investigation of it seriously.

GS 3: Do you recall the paper regarding weight loss in low fat v high fat? I predict in advance, if indeed low fat had better weight loss, then the high fat was not low carb (i.e. at least under 100g per day, and hopefully under 50g CHO/day). If it was, I would have more serious food for thought. What we are talking about is reducing massively the area under the daily insulin curve.

BS: CHECK IT OUT ABOVE. INSULIN IS A GREAT HORMONE WITH ITS FINGERS IN SO MANY METABOLIC PIES, BUT I THINK TOO MANY PEOPLE ATTRIBUTE TOO MUCH TO IT IN RELATION TO ENERGY BALANCE. ONLY SMALL RISES IN INSULIN ARE ENOUGH TO TURN OFF LIPOLYSIS, MORE IS NEEDED TO TURN OFF GLUCONEOGENSIS, MORE FOR GLUCOSE TRANSPORT INTO THE CELL AND EVEN MORE FOR DE NOVO LIPOGENESIS.

I agree, the problem is most people on a high carb diet are hyperinsulinemic the whole day.

SORRY TO QUOTE ALL THIS OLD STUFF BUT SEE KEVIN ACHESON’S PAPER AM J CLIN NUTR 1987http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=3799507

GS: As I expected, the Kendall paper wasn’t LCHF so isn’t relevant. The Acheson paper shows that subjects had a highly insulinemic response to dextrose – obese and non-obese alike. They showed very little de novo lipogenesis, even with large carb loads. OK. But, insulin still dials down lipolysis and promotes fat storage. De novo lipogenesis might only be a minor part in this. But that doesn’t mean insulin doesn’t promote weight gain through modifying energy metabolism, storage, and output.

Look, when insulin is raised a bit you turn off lipolysis and you store any fat floating around. That is exactly what happens in the standard industrial moderate carb moderate fat diet. Sugar through fructose increases insulin resistance. Other inflammation sets in making the problem worse. Leptin gets blocked. Hyperinsulinemia ensues well before actual glucose control is evident. Weight gain is a downward spiral and you are permanently stuck in the seasonal metabolic weight storage situation humans are well designed for.

GS: Thanks for talking to me about this. I am thinking about this very carefully. In some ways, I would like you to be right then I can carry on with what my career has followed so far, which is mostly environmental determinants of physical activity and obesity. But if the alternative hypothesis turns out then we have to rethink obesity prevention and treatment. At least that’s my view. If macronutrients, namely dietary carbs, overwhelm our biological capacity to deal with them in loads way beyond that which our ancestors (and therefore we) were designed for, then we should think carefully about that.

BS: THE HYPERCALORIC FOOD ENVIRONMENT (WHICH INCLUDES A HELL OF A LOT OF SIMPLE CARBS FOR SURE) IS WHAT OVERWHELMS US IN MY VIEW – SUGAR, FAT AND SALT MAKE FOOD MUCH EASIER TO OVERCONSUME. I DON’T THINK WE NEED TO HYPOTHESIZE SUCH FINE GRAINED MACRONUTRIENT EFFECTS

GS: I think we all agree that the industrial food culture and environment is toxic. Your argument has been that it’s too much food laying around, period. I disagree. That certainly doesn’t help. But simply processed carbs, especially sugar, are the active ingredient in this. Yes, taste added with fat and salt heightens palatability and promotes fatness. This is because it’s the carbs that stimulate the fat to be stored not burned. There are obviously issues about seed oils, trans fats etc as well. This is especially so in inflammation. Microbiome issues in absorption, gut permeability and inflammation are all mechanisms that are likely to be involved. Current literature puts dietary carbs, especially sugar and wheat (also highly processed oils), at the top of the list of suspects here, not saturated fat.

Again have a look at a later paper from your previous lab showing just how carbohydrate balance affects weight gain through subsequent food intake.

GS: I understand you think it almost certain I’m wrong, but that’s science and it might just be true.

BS: A HELL OF A LOT HAS ALREADY BEEN DONE IN THIS SPACE BUT I AM NOT REALLY UP WITH THE PLAY – JUST STICKING TO OLD IDEAS

GS: I think we can easily both agree that nutritional science and metabolism isn’t fully understood yet. Where we seem to disagree is how that rolls into public health. I SAY WE NEED TO THINK MORE CAREFULLY BECAUSE CARBS AFFECT SOME PEOPLE VERY ADVERSELY. You say that it’s just the presence of food in general. There seems to be a gap there in what this will mean for the person on the street. I say we need to think about nutrient composition and how this affects different people.

GS: It wouldn’t be the first time science got something wrong. I’d also challenge you in the spirit of medical self experimentation to try a LCHF diet, with ad lib quantities, for three weeks. Control dietary carbs to 50g/day and judge your own metabolic changes. I did for sceptic reasons and decided it needed more investigation….just a thought.

BS: I THINK IF I PAID ATTENTION TO MY DIET IN REDUCING CARBS OR FAT OR ALCOHOL I WOULD BE BETTER OFF. IF YOU TAKE STUFF THAT REPRESENTS ABOUT 30 OR 40% OF OUR DIET (IE BREAD, PASTA, RICE, SPUDS, ROOT VEGE, BISCUITS, CAKES, PASTRIES ETC) THEN MY GUESS IS THAT I WOULD DEFINITELY LOSE WEIGHT AND I WOULD FEEL BETTER FOR HAVING DROPPED A FEW KG.

GS: Medicine has a long history of self experimentation. Are you remotely curious about the possible physiologies of carbs and how that might affect you personally? As well, I am saying remove these and replace them. I’m saying replace them with fat. It’s not deprivation and undereating. It’s tasty and fun. More importantly it sets humans into an energy homeostasis that allows control over eating. What I don’t think you are considering is that different dietary intakes affect satisfaction, satiation, and health in different ways because they affect energy homeostasis in different ways. LCHF is quite different and has a biological mechanism for being different to other diets. It also is not a fad diet as it is the only one based on evolution by natural selection as a principal of shaping our human genome’s response to different macronutrients.

BS: GREAT TALKING WITH YOU BUT I HAD BETTER GET OUT OF THIS ENJOYABLE STUFF AND GET BACK TO MY NHMRC REVIEWS

GS: Did you see the paper written about NHMRC writing and reviewing showing the cost to the Australian tax payer compared to the investment? Something like 600 person years spent grant writing alone in the last round!

Subsequent comment form Tim Noakes, after reading the correspondence

Hi Grant,

Just a very quick comment. You burn what you eat. This is where the alternate argument breaks down. Carb burners eat high carb diets. If they get fat it is because they eat too much carbs (carb addiction) and are insulin resistant. Place them on a high fat diet (by removing ALL addictive carbs) and they lose weight and become powerful fat burners. Problem solved.
Boyd needs to get into clinical practice. Once he sees it happen once, he will understand. My best case – 80kg lost in 7 months. New man but same “metabolism”. So what changed? Learned to control his carb addiction.
From the literature you can select anything you want to support your argument. But when you are in practice, the evidence is absolutely clear. The only people who don’t understand are those who have never tried it.
Will respond more fully in due course.
Warm regards,
Tim