We’re doing a public lecture on Low Carb High Fat

Low Carb High Fat_16 Oct 2013

Click here for the full PDF version of the invite Low Carb High Fat_16 Oct 2013

Join me and my research team to see the latest in the world of Low Carb HIgh Fat (LCHF) research and practice.  We will look at what the research shows, what we are doing, and what this means in practical terms.  We will be discussing both health (weight loss, diabetes, and chronic disease), and athletic performance.

Get in quick to register if you are in Auckland as seats are free but limited.

When: Wednesday October 16th 7-8.30 PM

Where: AUT Millennium INstitute, Mairangi Bay Auckland

Register by emailing hpc@aut.ac.nz

More on low carb and diabetes

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Last week I wrote a short piece on low carb and diabetes, specifically Type 1 diabetes. That’s the diabetes where the body can’t produce insulin (aka Diabetes Mellitus or T1DM).

Conventional wisdom has it that people with T1DM should eat a decent amount of carbs (200+ grams a day), which is a fair bit, and you match the insulin you inject to cope with that carb load.  The trouble is that:

  1. It’s really hard to exactly match the insulin to the glucose load
  2. Operating like this means that you will be constantly hyperinsulinemic (high insulin) which causes long term damage to the diabetic.  This is the same problem that Type 2 diabetics have.  They are insulin resistant in the first instance, so they simply produce their own high insulin and that’s the health risk of Type 2 diabetes.

I also commented on a series on ABC’s Radio National Health Report. The item in the first week was an interview with Gary Taubes (well known author and low carb expert) and an interview with a Type 1 diabetic getting excellent outcomes on low carb.

The second week was a response form Dr Maartan Kamp a diabetes expert. He was completely condescending and paternalistic to the point of being embarrassing.  He said that he would never promote low carb diets for diabetics because people wanted to eat normally.

I am writing this blog because I have been surprised by  the voracity of the comments and emails I have received about the medical profession and diabetes. Common medical profession – do your reading and get your act together.  Snap out of it!

Here’s a note from a Type 1 diabetic

I’ve been type 1 since 1970 and my initial diabetic diet was relatively low-carb — at least compared with what in the Eighties was conventional wisdom. I spent decades eating cereal with skimmed milk and pasta with marinara sauce and being told by board-certified endocrinologists that I just needed more exercise and more insulin to get my hemoglobin A1c under 10.5 or so. The culmination was Symlin, an expensive synthetic relative of amylin that left me nauseated every waking moment but helped a little, partly by slowing digestion and partly by making me too nauseated to eat much. About five years ago I went low-carb and when I belatedly saw my endocrinologist he was pleased that my A1c was around 8 but insisted that the human brain cannot function on under 100g of dietary carbs a day. Now my A1c runs around 6.5 and I’m still overweight but my complications are getting no worse. My hatred for the American Diabetes Association is boundless.

Here’s one from a doctor practicing low carb with diabetes

Speaking from the coal face of General Practice, using a lower carb “real food” approach is incredibly successful in controlling type I DM. Done right, most end up on a smallish dose of long-acting insulin at night, with very little or no need for any short-acting boluses during the day. Great Hba1c, low triglycerides, high HDL. The only problem is the patient having to nod along to their endocrinologist and specialist nurse, and casually omit informing them of what they’re really doing. Sad state of affairs

Here a note from Catherine Crofts – a doctoral student and pharmacist who really got mad at the medical profession’s attitude.

Following up Maartan Kamp’s response to the people with diabetes not being advised to follow a low carbohydrate diet because it essentially limit their food choices raises some really interesting inconsistencies within the health field but also some important questions around informed choice.  With respect to dietary advice for people with diabetes, what he said was  “So what we attempt to do is actually allow people to continue to live their life the way they wish, eat the way they wish.”

People who suffer from gout (painful swelling in the joints, also known as gouty arthritis) are routinely recommended to avoid purine rich foods.  The alternative is to continually suffer from gout attacks that may lead to one or more joints being crippled.   Will this dietary change have significant social implications?  Almost undoubtedly – many men really grumble if you ask them to limit their bread, red meat and beer intake.  While medication can treat or prevent gout, the important point is these people are always given the information that changing their diet can reduce the frequency of gout attacks.   Whether they choose to follow the advice is up to them.

As a pharmacist, I have counselled many patients with this dietary advice and provided printed  information for them to take home – sometimes with graphic pictures with the consequences of untreated gout.   The threat of amputations, or not being able to run around with the children/grandchildren in the future can be a good motivator for change.

People with coeliac disease must avoid all foods containing gluten to avoid severe gastro-intestinal upset.  Again, these people are given strict counselling as to what foods they need to avoid and again, the consequences of what will happen if they don’t follow this advice.  People with coeliac disease usually become very good at avoiding all trace of gluten, (bread or anything with flour, wheat or some other grains, many processed foods).  I also get quizzed from some patients as to the presence of gluten in medications and other health products.

Children with severe epilepsy are often recommended to follow a very strict ketogenic diet as it is proven to reduce the risk of seizures.  Many of these children become seizure free and their parents go to some pretty extreme lengths to maintain this diet…now a lifestyle for them.

There are other examples, but these people cannot “continue to live their life the way they wish, eat the way they wish” if they want to stay healthy and disease free. 

Ironically, adults who develop late-onset seizures are not offered the same dietary treatment as children as for some reason adults are deemed by the medical profession to be unable to adhere to the dietary advice.   Sure, many won’t be able to as it is not easy, but surely they should be given the chance?

This brings in then the interesting question of informed consent.  People have to consent to having any medical treatment based on a clear understanding of the facts, implications and consequences both on for the immediate and future concerns.  Sufficient information needs to be provided to allow someone to make that informed consent.  If insufficient information is provided, it can raise some serious ethical questions.

What Dr Kamp said smacks of “let’s not tell the people of a possible non-drug option because they can’t stick to it, so we won’t even given them the chance to try”.  That attitude is simply condescending and paternalistic.  The bigger question is whether it is ethical?

I have to agree Catherine and so does someone on the ABC site:

Listening to Dr Kemp, one wonders how many patients with either type I or type II diabetes get the benefit of ‘informed consent’, so that before they rely on insulin, exercise and calorie reduction they are informed that a low carb diet is an optional pathway.

Awkward? Food blogger calls me “socially awkward”!

Me, Grant Schofield standing up for the high fat diet and good science
Me, Grant Schofield standing up for the high fat diet and good science

How is one supposed to feel?  Good, I think as friend, food blogger, and academic Dr Mikki Williden wrote a blog about me and others.  Read here.

Of note:

  1. She stands up for me, and the fact that challenging conventional nutrition science is worthwhile.  Thanks, as frankly I have hardly impressed the public health people I usually interact with in New Zealand.  They mostly assume I am either mad, stupid, ignorant or a combination of the three.  I, of course, think I’m on the right track.  And now at least Mikki does.  TICK
  2. She describes me as “He’s a strange mix of charismatic and socially awkward – which are not uncommon character traits for an academic“. I was giving this a big tick on the basis of the charismatic bit, but socially awkward – who knew?  I asked a few people about this, and pretty everyone except the ones I regard myself as socially awkward agreed and said that everyone knows this!  Oh well, that’s that.
  3. She writes “While he hasn’t devoted his entire academic life to studying the area, what I don’t think people realise is that Grant has literally spent the last year living and breathing the literature around insulin, carbohydrates and health (as anyone within earshot of him over this time can attest to). I would conservatively estimate he has crammed the same amount of information in that time that would take another person five years to learn.”  TICK and thanks for that.  You have to do your reading, its as simple as that.  I’m more impressed by Catherine Crofts my doctoral student who has read probably 1500 research papers in the last several months.
  4. Most importantly. she writes this which I really really like and agree with “He’s not always right – far from it, and he’s the first to say he is wrong when he is wrong. And his belief that the foundation of what we’ve hung our hat on in terms of health is flawed makes for some uncomfortable conversations. But, without people like Grant, we would not be having the conversations to begin with. In terms of public health I think we should be questioning – particularly with the health problems that most western nations suffer from today. And hopefully, instead of dismissing what he has to say as being uninformed, people will be doing their best to prove him wrong if they truly believe that what he has to say is inaccurate and misleading.

That last one is just so important, and as I have talked more and more about human metabolism and how our conventional dietary approaches have little scientific basis for the most afflicted – the obese and the diabetic – I have copped a bit (a lot?) of criticism.  But I not yet seeing is the compelling arguments from these public health (scientists).  Just criticisms.

Thanks Mikki for raising the attention to the cause of good nutrition and metabolic science.  We want good science and good debate.  I’m up for that.

Hopefully it won’t be too awkward!

 

 

Type 1 Diabetes and Low carb

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I met a guy called Ralph Norris a few months ago.  He is one of New Zealand’s more successful businessmen and corporate CEOs.  He’s had roles as CEO of Air New Zealand, ASBank, and Commonwealth Bank Australia (CBA).  He’s on the board of New Zealand’s biggest company Fonterra, and the Treasury board, and is fit and healthy looking. He’s a peak performer in every aspect of his life; even in his mid-sixties he still looks good and is sharper than anyone I know.

Oh yeah, it’s Sir Ralph Norris too!

I was showing him around our labs at AUT’s Millennium Institute where my research centre is.  I was explaining the work we do with both athletes and the general public to try to understand and encourage them to burn fat as a primary fuel source and how we often achieved that through low carbohydrate high fat (LCHF) diets. We talked about resetting the metabolism, lowering insulin, and dealing with Type 2 diabetes.

He immediately became engaged and explained how he had been working on his own diabetes (Type 1) for 20 years with a LCHF diet.  He described his glucose control as “the best his specialist had ever seen”.

This leads me to a question I am often asked about – are Type 1 diabetics safe to use a LCHF diet?

I think the first thing to remember is that Type 1 diabetics have no insulin.  As such, they cannot move glucose into the cells. Before synthetic insulin was invented, the disease was untreatable and sufferers would literally starve to death because fuel couldn’t move into the cells.  Either that or ketoacidosis would get them. This is a dangerous condition where the body produces so many ketone bodies that you end up with life endangering acid blood. Either way it was bad news.

Enter insulin. Now diabetics had the missing substance and could live a healthy life – almost.

The same thing applies to every human – high blood sugar and subsequent high insulin to deal with that sugar will directly and indirectly damage tissues and organs all around the body. These effects, through vascular and tissue damage are well documented in the scientific literature.

So how about we help the Type 1 diabetic by reducing and restricting the amount of carbohydrate they eat?

Sounds good to me, but when I asked others in the field about this they looked at me sternly and told me that I was simply out of line and WRONG.  Restricting carbs for Type 1 diabetics is dangerous they say.

How I ask?

Ketoacidosis and other complications they reply.

Really – damn – well I think THEY are just plain wrong and the research both mechanistic and experimental would support this.

Here’s a 2012 study by Nielsen et al in Diabetology and Metabolic Syndrome showing safety and great outcomes.

BACKGROUND
Reduction of dietary carbohydrates and corresponding insulin doses stabilizes and lowers mean blood glucose in individuals with type 1 diabetes within days. The long-term adherence for persons who have learned this technique is unknown. To assess adherence over 4 years in such a group the present audit was done retrospectively by record analysis for individuals who have attended an educational course. Adherence was assessed from HbA1c changes and individuals’ own reports.
FINDINGS
Altogether 48 persons with diabetes duration of 24 ± 12 years and HbA1c > = 6.1% (Mono-S; DCCT = 7.1%) attended the course. Mean HbA1c for all attendees was at start, at 3 months and 4 years 7.6% ± 1.0%, 6.3 ± 0.7%, 6.9 ± 1.0% respectively. The number of non-adherent persons was 25 (52%). HbA1c in this group was at start, at 3 months and 4 years: 7.5 ±1.1%, 6.5 ± 0.8%, 7.4 ± 0.9%. In the group of 23 (48%) adherent persons mean HbA1c was at start, at 3 months and 4 years 7.7 ± 1.0%, 6.4 ± 0.9%, 6.4 ± 0.8%.
CONCLUSION
Attending an educational course on dietary carbohydrate reduction and corresponding insulin reduction in type 1 diabetes gave lasting improvement. About half of the individuals adhered to the program after 4 years. The method may be useful in informed and motivated persons with type 1 diabetes. The number needed to treat to have lasting effect in 1 was 2.

Even more interesting is a recent interview conducted by Dr Norman Swan on the ABC’s Radio National programme ‘Health Report’. Dr Swan is an excellent health journalist and just picked up on the whole low carb thing.  I highly recommend listening to this if you are a Type 1 diabetic, or you know one.

Check the response by endocrinologist Dr Kemp on ABC Radio National to the diabetes story.  Dr Kemp, who is a senior endocrinologist and past president of Diabetes Australia, is out to lunch and completely misses the point.  Here is a great example when he says why he wouldn’t point patients with diabetes to a low carb diet….“So what we attempt to do is actually allow people to continue to live their life the way they wish, eat the way they wish.”

The listeners however – and those who have made comments on the Radio National www site – get it. These are lay public afflicted by diabetes. Will the medical profession be the last to understand the problem they are charged with treating? Here’s an example comment

So this expert agrees that low carb diets control blood sugar and reduce the need for insulin (which is incredibly good for everyones health) but he wouldnt recommend that diabetics eat a low carb diet because it would be too difficult for them to stick to…I think that is a condescending and ridiculous thing to say. Is it easier for those people to have their feet amputated, get vascular disease, go blind and need dialysis? I know what it does represent – diabetics who continue to eat a high carb diet will need prescription medication and a raft of medical interventions for the rest of their lives – very prosperous for some. There is no money in dietary interventions – especially nutrient dense fresh wholefoods. I feel very sad for all the people out there who rely on this experts advice for their health and their lives.

Footnote: Another Vanuatu story.  I have written previously about some of my experiences doing diabetes prevention work in Vanuatu and other places around the Pacific. I now recall a very sad story of a beautiful 19 year old girl in Southern Vanuatu. I was testing fasting blood glucose and hers came out at 26 mmol/l (normal = less than 5). Straight way I knew she had Type 1 diabetes recently developed.  I sent her away and tested her again the next day, same thing, and again the next day, same again.  What breaks my heart here is that there is simply no insulin on those islands and virtually no chance of getting any. So she was just going to be left to slowly die with Type 1 diabetes, something we treat everyday in New Zealand.  It’s hard to go away from there and feel good about anything…..

Comparing LCHF and the Mediterranean diet

Spot the difference

By Helen Kilding and Grant Schofield

We’ve been hearing quite a lot about how healthy the Mediterranean diet is.  So what is it, and how does it compare with the Low Carb, High Fat (LCHF) approach that we talk about on here?  How different are they and why would you choose one over another?
Let’s find out.
The traditional Mediterranean diet is characterised by a high intake of olive oil, fruit, nuts, vegetables, and cereals; a moderate intake of fish and poultry; a low intake of animal products like dairy, red meat, processed meats, sugar and sweets; and wine in moderation and consumed with meals.
 
The LCHF diet is characterised by a high intake of natural fats (including olive oil, but also other healthy fats such as butter and coconut oil), a similarly high intake of vegetables, but limited fruit and no cereals. Why limited fruit? Fruit is nature’s candy, with a medium sized apple containing the equivalent of 3 teaspoons of sugar. Sure, in it’s natural form, fruit is a good source of fibre and some vitamins, but so too are vegetables, and with less of the sugar hit. 
 
And why no cereals? Well despite what we’ve been lead to believe, there is no good reason to eat cereals, even wholegrain. The fibre argument and the vitamin and mineral argument just don’t stack up – a plate of salad or veggies packs a much bigger and better fibre and vitamin/mineral punch than any cereal. And whether we need more fibre in our diet is debatable anyway. But cereals are cheap and highly lucrative. The corn industry has a lot to lose if/when the truth gets out. As Christine Cronau (author of The Fat Revolution) nicely describes, “a breakfast of eggs and butter is packed full of Vitamins A, B, D, E and K, along with iron, zinc, calcium, lecithin, iodine and more. Adding some unrefined salt adds a further 84 minerals and a fried tomato a healthy dose of vitamin C”. Beat that cereal!
 
The fact is humans are not adapted to consuming cereals and they are full of toxic anti-nutrients (lectins, gluten and phytates) that we don’t have the ability to deal with. Lectins bind to insulin receptors and the human intestinal lining and cause leptin resistance, which as regular readers of this blog will know, accelerates metabolic syndrome independently of obesity. Gluten (found in wheat, rye and barley) might be even worse and certainly is more widely known. Around 1% of the population are celiacs (completely intolerant of gluten) but it’s not just celiacs who suffer the damaging effects of gluten. And finally phytates, make the very minerals that whole grains and cereals supposedly provide us with, bio-unavailable. Awesome!
 
But getting back to our comparison, a moderate intake of fish and poultry is common to both diets, as is a low intake of processed meat, and wine in moderation. So the last big difference really is in the red meat, cheese, eggs and sugar. Whereas the Mediterranean diet supports low intake of all four, LCHF promotes unlimited consumption of meat, eggs and cheese and no consumption of sugar.
 
The health concerns around meat and eggs, particularly in relation to cholesterol, are unfounded and indeed animal proteins and fats, like eggs and butter, contain many of the nutrients missing in modern Western diets. With the Mediterranean diet, around 25-35% of calories come from fat (8% or less from saturated) compared to around 70-80% on LCHF. With the latter, the body learns to use fat for fuel instead of sugar (read more about fat adaptation here). If fat intake is too low, this cannot occur, so regardless of whether you are carbohydrate sensitive or not, if you want to become a fat burning machine, for endurance performance, weight management or improved cognitive function, LCHF rather than the Mediterranean diet is the way to go. Remember though, fat intake should only be high if carb intake is low – high intake of both is not OK! 

Can you be a healthy endurance athlete?

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I’ve been getting quite a few questions about triathlon and other endurance sport training and racing.  Even in our own research group, there is a lot of debate and questions about what and how, especially regarding supplemental carb use.

I think it comes down to understanding that ‘high performance endurance athletics’ and ‘health’ are not always the same thing.  I might even go as far as to say that they are mostly mutually exclusive in the long run.

That’s different from doing endurance events and being healthy – I believe that is possible.

Most of my friends are not going to like hearing this…and after a life of pursuing carb-fuelled high performance endurance, why have I changed my mind?  And what should you do if you like being involved in endurance sport and exercise but want to maximize your health and avoid things like heart damage and self-oxidizing yourself into early aging.

I’ve been an advocate recently for the polarized training approach – where you spend most of your time doing very easy aerobic, fat burning exercise, and just a short amount of time doing very  high intensity training.  You try and avoid that middle chronic cardio zone.

Case study 1: Joe McQuillan, endurance exercise physiologist and low carb high fat (LCHF) proponent.  He is happy enough himself to be on a LCHF diet because of the energy and weight benefits, but he’s not convinced that a polarized training approach (also known as an 80/20 approach) generates any sort of high performance for competitive endurance athletes.

We just finished a long discussion about this where Joe points to the “optimal” training points for endurance performance.  Here’s his note below on this.

Grant, this modified table (below) is from Racing and Training with a power Meter by Coggan and Allen. All I have done is arrange the outcomes by way of 1st and 2nd contribution to enhancement of that outcome. FYI L3 is tempo, L4 threshold, L5 VO2max, L6 anaerobic (<3 mins). Nowhere on the list is L2, for most it falls as the 3rd most important zone to contribute changes to an outcome of X. This does not detract from the fact we need to do L2 exercise and a lot of it for base work, but within L3/L4/L5 sessions we spend time in this (L2) zone, + warm-up and cool down from interval training increases this by default. I think in certain phases for a road cyclist and 1/2 IM/standard dist triathlete a 50/50% <L2/>L2 is likely.  

 I don’t see 80/20 as a valid method for enhancing performance at L3/L4 racing (I also saw this recently appear as 75/25).

 Expected Outcomes

1st Priority

2nd Priority

Increased plasma volume (L4 & 5)

4

5

Increased muscle mitochondrial enzymes (L3 & 4)

4

3

Increased lactate threshold (L3 & 4)

4

3

Increased muscle glycogen storage (L3 & 4)

3

4

Hypertrophy of slow twitch muscle fibres (L5)

5

3/4

Increased muscle capillarization (L3)

5

3/4

Interconversion of fast twitch muscle fibres (type IIb -> type IIa) (L3 & 4)

3

4

Increased stroke volume/maximal cardiac output (L4 & 5)

5

3

Increased VO2 Max (L3 & 4)

5

3

Increased muscle high energy phosphate (ATP/PCr) Stores (L6 & 7)

7

6

Increased anaerobic capacity (“lactate tolerance”) (L6)

6

5/7

Hypertrophy of fast twitch fibres (L7)

7

6

Increased neuromuscular power (L3)

7

6

In other words, the best race results for an athlete can’t easily be obtained from mostly easy training with some occasional harder stuff.

Is Joe right? Well the more of the higher intensity training you can get AND adapt to then the faster you will probably end up going. This is similar to what Mark Sisson talked about in his blog this week – it’s a matter of time frames and perspective on performance. Long-term health eventually matters to long-term athletes too.

The thing is that short-term or even medium-term maximum performance doesn’t take into account overall wellbeing and health – which applies long-term both to elite athletes and weekend warriors.

There is only so much moderate to high intensity training you can take.  So my feeling is that most people should be very careful about overdoing this.

Believe me, I have been there done that as far as overdoing it is concerned. It’s still something I constantly struggle with – exercise makes me feel good and I like so many aspects of it, including the social.  But the toxic effect of too much intense exercise is something I have to try and avoid for my own good.

This of course means that I won’t be competing with and beating people who I likely could, simply on the basis of our pre-training physical abilities.

That’s a bummer, but that’s the way it goes.  Some guys will always smash themselves up a bit, optimize their performance, choosing to neglect their long-term health. They will be the ones on the age group podium.

Should we celebrate this? Probably at the Olympics and world championships we enjoy seeing what the limit for humans is.  But, in my opinion, that shouldn’t be what non-professional athletes celebrate. If you want to do that, then do it in small controlled amounts and take a break.

Health, as I have written about previously, is about the application of stress and your adaptation to it. Too much stress is toxic. My opinion is that 20 hours of triathlon training a week is likely to be too much for most people who are working full time and might have other commitments – e.g. family, work, etc.

I guess that’s why you see a good deal of podium triathletes at triathlon age group world championships are professional coaches or independently wealthy and not working.  It’s only under these special conditions that you can tolerate the training stress and recover from it. Even then, that isn’t the optimal health outcome.

So if you’ve made your personal decision about endurance sport and health – and it is about personal health and wellbeing first, performance second – how should you proceed?

The balance between health and performance?

Case study 2: Julie, an older female triathlete

My goals are to get and hold my weight to or just under 60 Kgs and get my running improved. Current weight 61 Kgs. Generally in a tri I struggle to keep my 10km run under 55 mins. For my age group I am usually in the first 20% of the swim 10% in the bike and 50% with the run. I end up with a final placing in the first 5.

 I followed a schedule of about 18 hours training a week leading into the Auckland ITU (world champs). Aged 59 and came 10th.

 I will look to start Tri’s this summer. I have had a year off after 10 years competing.

Here’s my suggestion – give or take for the best balance between stress, enjoyment, health, weight management and energy.  Just a guide and flexibility is important.

First: Nutrition – Accessing and using aerobic lipolysis (fat burning) during the bulk of your training is crucial.  It produces less oxidative stress, tires you out less, requires less effort, and your brain and body operate more efficiently.  For this I suggest a whole food Paleo style diet with a degree of carbohydrate restriction – preferably off all sugar and grains. The amount of carb restriction depends on your tolerance to carbs and exactly how much glycogen you are burning in training. Dr Peter Attia has recently written a nice piece on calculating this. I prefer the full low carb high fat approach in a whole foods framework. That works well for me.

Just to reiterate, you need to get the nutrition right first.  No amount of training properly can make up for setting yourself down the sugar burning/addiction pathway.

Also, remember the exercise isn’t the thing that helps you make your goal weight – the nutrition does this.

Second: Training – I suggest capping things at 10 hours a week, maybe 12 if you have to. Remember it is adapting to the training that is important.  You won’t race at your absolute best, but you will be most of the way there. Exercise is a potentially toxic stimulus to your body. You want just enough in the context of the rest of the stress in your life to be able to adapt to it. Better under-doing it than over-doing it.

The bulk of the training is easy aerobic L1, L2, occasionally a little L4-5 where it can’t be avoided (going up a hill on a bike).  I’d do virtually all sessions in this zone, except 2 maybe 3 a week where I’d do some very short and very hard interval sessions like the ones below.

Sessions:

  • Run track 10 by 1 min with 1 min rest.
  • Bike: 2 by 6 by 40 sec hard out, 40 sec rest
  • Swim: 10-15 by 50 m

This makes it very easy to design a program, you spend 10-12 hours in a combination of swimming, biking and running at easy aerobic pace.  You throw in very short sessions when you feel up to it, where you maximally hit out.

That, in my opinion, is the way to health.  It’s not the way to the best possible race performance though.  Your call.

Thanks as always to the super diligent Helen Kilding for her editing

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.

Does carb burning age you?

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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) Continue reading “Does carb burning age you?”

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

Do diabetes specialists have learning resistance?

The healthy diabetes plate is a peer-reviewed “evidence based guidelines for healthy eating for Type 2 diabetics”.PCD41A12s01

Here’s my rant around what I consider to be a gaping hole in sensible logic.

Here’s the biological logic:

  1. You have become metabolically dysregulated. In mainstream medicine, your doctor will call you “insulin resistant”.
  2. That means your body is having difficulty getting glucose out of your blood stream into your cells.
  3. Your body still needs to get rid of this glucose, so your pancreas produces more insulin to get the glucose into the cells.
  4. Chronically high insulin makes you more insulin resistant, requiring you to produce more and more insulin. It gets worse and worse. Fat oxidation is turned off, and adipocyctes (fat cells) take up extra glucose and fat.
  5. No matter how much insulin you produce, you can’t move all the glucose into cells. Your blood glucose is high which damages the body irreparably.
  6. Sometimes, because of the stress of overproduction of insulin, the pancreas will have burnout in the beta cells which produce the insulin. Then you’ll need extra insulin, like a Type 1 diabetic.

Here’s your choice:

  1. Take mainstream diabetes treatment advice and follow their dietary guidelines (see above and below). That will be a low fat, moderate carb diet, where you should probably restrict calories. This will result in continued high blood glucose and insulin as you are eating quite a lot of carbs. Whole grains and beans are suggested as they are higher quality and absorbed more slowly. That just means high insulin the whole day for the insulin resistant person. I’ve written about the evidence for this previously.
  2. OR Here’s a novel idea…..or am I missing something here all you diabetes specialists and dieticians? RESTRICT YOUR DIETARY CARBS to very low amounts (<50g/day), eat more fat, and everything will improve. Here’s the outcomes when you do this.
    Just a thought. A glaringly obvious solution to the problem of being unable to tolerate carbs and move them into cells……don’t eat them!

    Take a look at the diabetes food pyramid below…..a low fat diet will be a high carb diet, even with high lean protein, because excess protein ends up being dealt with in exactly the same way as carbs. I contend the only way that a diet like this can work to help a diabetic is if somehow they have enough will power to semi-starve themselves into a very low calorie diet. That diet now works because it too is now a low carbohydrate diet. Why does mainstream medicine seem to be so resistant to even considering this possibility? Who’s right here? Do I have learning resistance, or do the current guidelines just make no sense in the light of the evidence? Insulin resistance or learning resistance?

    pyramid