The real food guidelines

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It’s a food fight.

The time has finally come where a deep and important line needs to be drawn in the sand.  No more throwing bad science and bad advice around.  Stop!

The “food pyramid” guidelines are still alive (and well?) in New Zealand (see here). They are outdated, old school and quite simply wrong. Recently they were up for review…

Unfortunately, they came back more or less the same – saturated fat and fats in general are bad for us ….blah blah blah.

So our team felt we had to put all the science out there publicly for everyone to have a look at. So here it is for your scrutiny.

MOH dietary guidelines feedback REVISED Appendix 9.5.14

 

This is our response to the draft nutrition guidelines.

The timing could not be better actually as tonight I go head to head with the very people who advised on these guidelines.  The 3rd Degree piece will be available here (its rightly called “Food fight” after 8.30 tonight NZ time.

Please take the time to read at least the lay summary, and even the full scientific document. I think you will be shocked just how little there is to back up the current and future nutrition guidelines.

It’s time for a full and robust scientific analysis of what we are told to eat to be presented to government health officials (who have it now), and the lay, scientific, and health communities.

We have also proposed a new set of guidelines called the Real food guidelines – real food, for real people, based on real evidence.  It’s time to get real people!  Here they are for the first time :

The real food guidelines
Real food for real people, based on real evidence

  1. Enjoy nutritious foods everyday including plenty of fresh vegetables and fruit.
  2. Buy and prepare food from whole unprocessed sources of dairy, nuts, seeds, eggs, meat, fish and poultry.
  3. Keep sugar, added sugars, and processed foods to a minimum in all foods and drinks.
  4. If you drink alcohol, keep your intake low. Don’t drink if you are pregnant or planning to become pregnant.
  5. Prepare, cook, and eat minimally processed traditional foods with family, friends, and your community.
  6. Discretionary calories (energy foods) should:
    a) Favour minimally refined grains and legumes, properly prepared, over refined or processed versions, and boiled or baked potatoes, kumara or taro over deep fried or processed potato fries and chips.
    b) Favour traditional oils, fats and spreads over refined and processed versions.

We welcome feedback and scrutiny of our scientific analysis. This is open source and for the people. We are constantly trying to improve our understanding of  the science of human nutrition. The evidence changes all the time. Our scientific statement is another iteration in the right direction but should by no means be where we stop.  It’s a start..

Thanks to everyone in our team who contributed (see below).  Also Dee Holdsworth-Parks for tirelessly keeping my life organised and our team working smoothly.

Dr Caryn Zinn PhD
NZ Registered Dietician. Senior lecturer Human Potential Centre, AUT University

Dr Nigel Harris PhD, BRmgmt
Senior lecturer, Human Potential Centre, AUT University

Dr Mikki Williden PhD
Registered Nutritionist, Senior lecturer Human Potential Centre, AUT University

Catherine Crofts MPS M.Phil
Research Assistant, Human Potential Centre, AUT University

Dr Simon Thornley BHB, MBChB, MPH (Hons), FAFPHM.
Professional Teaching Fellow & Research Fellow, Section of Epidemiology & Biostatistics, University of Auckland

Cliff Harvey ND
Holistic Performance Nutrition

George D. Henderson
Research Assistant, Human Potential Centre, AUT University

LCHF success, but will protein kill me?

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Here’s a great letter about LCHF success but with an important question. I hope you enjoy Norman’s story – it’s a nice one about improved weight, energy and health.  Great blood results, but some concern about protein. In fact, its been a big week for protein.  The story about two research papers lead to headlines like “High protein as bad as smoking” (see detailed comments I’ve made at the end of this blog).

So today we’ll look at Norman’s story, and think about the role of protein.

Hi Grant,

Following the recent post on your blog from Andrew, I thought I would share my indicators and also raise a question.

I am a 51-year-old male and switched to a LCHF diet just over 6 months ago. When I started the new eating regime I weighed 93kg with a BMI of 27.5, now I weigh 86kg and have a BMI of 25.4. I lost weight rapidly at first, losing 5kg in the first 2 months. Weight loss then slowed, and rose slightly over the Christmas holidays (Mince tarts and Christmas pudding being my undoing!) but since late January has again continued a slow downward trend.  In terms of getting a healthy BMI I would like to get down to about 80kg, which would place my BMI at 23.7.

While weight loss was my first goal, I was also concerned about my overall health because I have always had a ‘sweet tooth’. When my older brother was diagnosed as pre-diabetic a couple of years ago, I was concerned about going the same way. Two years ago I had a badly infected gall bladder removed, a 4-week period of my life when I quickly lost 10kg (From 98kg to 88kg). I had hoped to keep that weight off, but despite being ‘good’ about portion sizes and snacking between meals I found my weight just crept up again over the ensuing year and a half. Then I discovered LCHF.

For breakfasts I have settled on a fruit salad with a sprinkling of nuts (Pure Delish’s “No Grain-ola” is my current favourite) and cream. While the fruit has a relatively high amount of sugar, I consider the nutrients in fresh fruit outweighs the disadvantages, and this sets me up for the day. About twice a week I have fried bacon and eggs for breakfast instead.  For lunch I have a handful of nuts, or about 100gm of hot roast meat from the local deli. Occasionally I have salami and cheese or similar. For dinner I usually have a home-cooked meat-and-veg meal, with only low carbohydrate veges. During the day I seldom snack, but have a couple of coffees with cream. I also drink 500ml of full-cream milk mid-afternoons (which causes many comments at work!). About twice a week I will have an Atkins-diet snack bar, which has high fat and a few grams of sugar. I also succumb to iced coffee’s a few times a week (despite knowing they are high in sugar!). So I probably have slightly more sugar than the ideal, but as long as I feel good and the weight is very slowly still dropping I am happy.

What has amazed me about the past six months is how my ‘sweet tooth’ has disappeared. When people at work bring cakes or chocolate I have actually no desire to have any, and that is not just self-discipline. When I was coerced into eating some chocolate some weeks ago I found it unbearably sweet and stopped after a single piece. Like Andrew, I am not hungry during the day (in fact am seldom hungry at all, even at mealtimes. I eat meals because it is mealtimes, not because my stomach is grumbling). During the day I find myself having to avoid snacking just for something to do – the mid-morning coffee break and muffin was a welcome distraction, and is not quite as distracting with just a coffee. Yet I have plenty of energy and have eliminated the three-thirty-itis that for years has been a common feature of my working days. I feel great, and enjoy my meals.

I have just recently had a full set of blood tests done as part of an insurance medical , and was able to compare them to the results I had from 2011. My indicators are as follows:

Oct 2011 Feb 2014
Total Cholesterol 4.8 5.0
Triglyceride 2.6 1.2
HDL: 1.11 1.31
LDL: 2.5 3.1
Chol/HDL Ratio: 4.3 3.8
TG/HDL ratio 2.34 0.92
Hba1C: 34 35

All of which are well within the ‘good’ limits, especially my TG.HDL ratio. The biggest change I note is my triglycerides have halved, and as a result my TG/HDL ratio is also dramatically better.

However, during my medical exam this morning I also had a urine test. This showed some evidence of proteins in my urine. My GP said that some recent studies had showed that higher protein levels have been shown to have long-term health issues. Although I am not specifically increasing my protein intake on LCHF, the nature of it means for example that for lunch I may have a slice of hot roast ham (with crackling!) whereas before I would perhaps have had a carb-laden muffin.So it is conceivable that my protein intake has increased overall, since most high fat snacks also contain a fair amount of protein.

Any comments on the protein indicator in the urine test? My GP is not convinced that LCHF is necessarily a good diet, although concedes my weight loss and all the indicators show it is working well for me. I have to say he is a bit old-school, like much of the medical fraternity, but I am working on him.

Thanks,

Norman Holtzhausen

First up – nice work Norman.  Love it and thanks for sharing. Let’s have a think about protein.

So what about protein?

What we do know about protein:

  1. Protein is essential for life. We need to derive most of it from diet including at least some animal sources
  2. Over consuming protein means extra glucose as the liver, through gluconeogenesis, turns that protein into carbohydrate. This may be a factor in some people stalling or not losing weight on LCHF diets – they are over-consuming protein and still giving the body a high glucose load, raising insulin and all the downstream metabolic effects.
  3. Protein is associated with the production of Insulin-like Growth Factor 1 (IGF-1). IGF-1 is necessary for life, but over  production may be part of the causal pathway for all metabolic diseases.
  4. People with kidney disease may need to be careful about over consuming protein as this can cause protein toxicity. Protein toxicity occurs when the body is unable to get rid of the potentially toxic wastes that are generated as a result of protein metabolism. Several studies, however, have found no evidence of protein toxicity due to high protein intakes on kidney function in healthy people.

So, I think that all means that if you are on a low carb eating plan, it’s best to be careful about overeating protein if you are prone to being insulin resistant. If you have any kidney disease then its even more important. I keep an eye on my intake from time to time using online apps like easy diet diary. I  have a tendency to eat too much protein and need to watch this.

What about the recent research showing that high protein intake is “as dangerous as smoking”?

There’s been a big deal in the last 10 days made about two studies in the journal “Cell Metabolism”. It’s all about the over-consumption of protein and mortality, especially from cancer.

The first was titled “Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population

They claim to show that:

  • High protein intake is linked to increased cancer, diabetes, and overall mortality
  • High IGF-1 levels increased the relationship between mortality and high protein
  • Higher protein consumption may be protective for older adults
  • Plant-derived proteins are associated with lower mortality than animal-derived proteins

My take: First, this is a cross sectional study and can never show cause and effect.  It may be that higher protein intake produces more IGF-1 and affects tumour growth and the development of other metabolic issues. That’s one reason why we advocate an adequate protein diet (around a gram of protein/kg per day plus a bit more if your are very active or doing resistance training).  Second, carbs also raise IGF-1.  So the logical best diet to reduce levels of IGF-1 being chronically high is a low carb high fat diet with adequate protein (exactly what I advocate for).

That said, this study can build a hypothesis which can be tested in trials.  It’s not the basis for public health recommendations. Another example of nutrition science headlines going beyond the data. Remember that across the WHOLE population in this study, there was NO effect of protein, AND only an ASSOCIATION in a sub-group analysis. Let’s not draw too much out of this study.  They probably are onto something about excessive IGF-1, which is great to see as we have been talking about that for a while.

The second was  titled “The Ratio of Macronutrients, Not Caloric Intake, Dictates Cardiometabolic Health, Aging, and Longevity in Ad Libitum-Fed Mice

They claim to show that:

  • Food intake is regulated primarily by dietary protein and carbohydrate
  • Low-protein, high-carbohydrate diets are associated with the longest lifespans
  • Energy reduction from high-protein diets or dietary dilution does not extend life
  • Diet influences hepatic mTOR via branched-chain amino acids and glucose

This study was a mouse model and in my opinion went well beyond their data and made conclusions that were simply not robust.  A few things worth noting. First. hidden in the supplementary material we see that they only report 25 of the 30 diets because they culled diets for mice who “failed to thrive” and were removed from the study (see more below).  Second, they fed them synthetic food made from soybean oil, two amino acids, sucrose and dextrose. Third, they didn’t report median life expectancy as the main outcome when they should have.  Last, mice have a different carbohydrate and protein metabolism to humans so extrapolating to human life expectancy is a long shot.

Here are some comments on the  study spotted by the vigilant (and more robust apparently) lay peer review process (Rory Robertson from the Ozparadox.com in this case).

  • Why were 100+ sick mice – all on low-protein diets – excluded from longevity results?
  • The original study reportedly involved 30 diets and nearly 1000 mice: see here. Yet the published paper reports the results for – amongst other things – “…longevity in [only 858] mice fed one of [only] 25 diets ad libitum”.
  • I’m trying to understand why five of the 30 original diets – all low-protein diets – were excluded from the final results.
  • Specifically, “These diets were discontinued due to weight loss (≥ 20%), rectal prolapse or failure to thrive”: Table S1, p. 7 
  • Failure to thrive! Imagine the disappointment of those 100+ sick/dying mice – ALL on low-protein diets – when they were told that, sorry, we’re going to euthanize you and then exclude you from this longevity study.
  • It’s a longevity study – sick and dying mice are the main thing we are looking for! Yet they were excluded. Why?
  • My observation is that the study’s high-profile “finding” – that lower-protein diets boost longevity in mice – is NOT ROBUST when the analysis is properly REBALANCED – by excluding the five most-unhealthy high-protein diets – to properly adjust the design for the low-profile exclusion of the most-unhealthy low-protein diets.
  • Moreover, to properly capture the underlying reality of the published results, it makes sense to focus on MEDIAN not maximum lifespans.
  • Checking the medians for the remaining 20 diets, the claimed boost to mouse longevity from low-protein diets has disappeared: the TOP-2 diets now are HIGH-protein, as are FOUR of the TOP-7 diets.
  • And LOW-protein diets now represent THREE of the Bottom-6 diets. (This information is via Table S2 in the link above.)
  • Doesn’t ditching those five obviously unhealthy low-protein diets – involving 100+ sick/dying mice! – by itself invalidate the paper’s claim that low-protein diets boost longevity in mice (and so humans)?
  • In my opinion, the study’s longevity “findings” should be re-written to properly reflect the underlying results from ALL of those original 30 diets, including the longevity of ALL those nearly 1000 mice.
  • As things stand, the public is being misinformed by this research claims and interpretation.

Take homes:

  • Science media is a mess, especially in nutrition, and you will have to do some research to make any informed choice.
  • Protein is essential for life, but over-consumption might be an issue – we still don’t have the full answer.
  • In my view, eating whole plants and animals provides about adequate protein and nutrient dense food to make thinsg work for most people most of the time. This is also lowish in carbs, and higher in fat.

Dr Caryn Zinn talks LCHF and dietetics – a must watch

This is an outstanding 15 min presentation by our own Dr Caryn Zinn, Registered Dietician, about her growth , development, practice and ethics of LCHF practice.  Recorded at the recent Low Carb Down Under conference in Auckland, she is the first of the videos released. Enjoy.  Send this to your dietician friends (and even the ones who are not friends!). Click here or below.

NZ’s health leaders respond to our research publicity: Saturated fat…its bad, low carb radical and unsafe

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It was no surprise to see this one coming.  A perfect storm for the old powers that be in New Zealand obesity research and practice. The BMJ paper on why we got the saturated fat thing wrong, the ABC Catalyst series, and me out and about in the media talking about low carb high fat. I just noticed another one the NZ Herald just now by a NZ dietitian.
Looks like I (and those associated with me, sorry everyone) are now officially on the outer after this press release today (see this Experts decry fat diet – press release from the University of Otago (Professor Jim Mann)). It’s undersigned by key members of virtually every health organisation in the country.
I guess they are thinking that this document will shut everyone up, calm the uneducated masses, and we can continue our solution to the world’s problem with chronic disease?  How’s that going by the way?
I know you’d like me and my team to go away, but it’s not happening. Sorry for the inconvenience. Oh, and because of the Internet and open access science, the public is now able to do its own research.  And guess what? It has decided that the evidence isn’t convincing either. The world has changed.
The science of nutrition and chronic disease, and the public health approaches to nutrition are not solved. Let’s just get that straight – we (my team) don’t have all the answers, and neither do you.  I’ve been wrong before and could be wrong again, the reverse also applies guys.  Things will change.  Change is happening now.  It will happen again in the future.
Jim, do you recall being the younger scientist taking on the older ones in the BMJ 1979 in “Fats and atheroma: A retrial?”  Back then you were arguing about the complexity of nutrition and the need to go beyond fat and think about refined and processed carbohydrates. Everyone here has more in common than not.
For the record, I did correspond with Jim Mann yesterday.  Here’s part of what I sent him.  I think it puts down a reasonable position.
Jim…….My take is that I haven’t particularly been walking around promoting saturated fat (although to be fair I haven’t been talking about reducing it).  I have been walking around talking about diets higher in fat and lower in refined and processed carbohydrates.  I think I have some sound scientific reasons for this.  I will continue the line of research for the foreseeable future. I haven’t done much on athletes as they said in the paper.  Most of the recent work is secondary analysis of a few very large datasets we have from the US in hyperinsulinaemia. Also some basic work in low carb high fat eating.  So don’t believe everything you read in the newspaper. We do have a reasonable line of research going across this topic.
 What, in my view, we (all) have in common:
  1. That whole plants and animals are likely to be good for you and your chronic disease risk
  2. That foods which reduce inflammation are good for reducing chronic disease
  3. That sugar and processed carbs are not good, especially if you are insulin resistant (most of the vulnerable populations)
  4. That hyperinsulinaemia and chronic inflammation (both highly inter-related and can cause one another) are a problem and part of the mechanism for developing CVD and other chronic diseases.
  5. The Standard American industrial food diet and lifestyle is toxic, and much of the research showing different ways of eating show benefits simply because this diet is so bad.
  6. Trans fats and high omega 6 seed oils are inflammatory
  7. The interplay between hormonal physiology, built environment, food, and physical activity is complex.  This influences catabolic and anabolic states and therefore human energy homeostasis.  We don’t know exactly how the system works.  We have made the mistake (using Einstein’s words “make it as simple as possible but no simpler”) to describe the calories in and calories out dogma which we need to move on from.
What we seem to disagree on is:
  1. That SFA from whole healthy animals has any proven negative effect on human health in the context of the above (whole food eating).
  2. Attributing changes in populations to specific nutrients in a complex multifactorial disease using epidemiology which measures eating is fraught and is giving answers the opposite to those observed in decent robust RCTs.
  3. That low carb high fats diets are safe, efficacious, and useful for the public.

My response to the technical points in the media release asking for evidence today

  1. The actual trials showing SFA reduction and health improvements are fraught because they are still mainly in the Standard American Diet (SAD) paradigm with small dietary modifications.  I agree that SFA intake in the context of the SAD might be problematic.  What I still have a problem with, in these trials, is that many (most) still use a control group eating the same old food.  Putting anyone on a diet different from the SAD will probably help.  Here’s the latest meta analysis.  In fact, the reality is that consuming SFA has positive effects on HDL cholesterol and reduces triglycerides.
  2. I’m not bothering with an in-depth rebuttal of the population studies.  There’s just too much (uncontrolled and unmeasured) going on there, with poor food measurement to say saturated fat causes anything.
  3. I particularly draw to your attention to the bit in the media release directed straight at me (just say my name guys I am comfortable with that). “However, the group suggests that those who advocate for radical new dietary approaches have a responsibility to provide convincing peer-reviewed evidence of long term benefit as well as absence of harm. Such evidence does not exist for diets high in saturated and total fat, and very low in carbohydrate”. I have tried to address these issues in depth below. But first, how a diet full of whole plants and animals, similar to what humans have eaten the whole time they have been on the planet (up until recently, when human life expectancy halved (agricultural revolution) and then got full of disability from chronic disease (last few decades)) is radical is beyond my reasoning.  Read the latest nutritional biochemistry and draw your own conclusions.
  4. Low carbohydrate diets being safe, efficacious and useful? RCT and mechanistic evidence shows that dietary saturated fat alone, in the context of a low carb diet doesn’t have the proposed cardio-metabolic risk effects of being harmful.  In fact, things all go the other way (improve) which is a very good sign.  I have put some references below, but also here’s a  recent meta analysis of the clinical trials of low carb high fat diets and their metabolic effects. People generally do better metabolically, adhere better, and control blood glucose and insulin better on low carb high fat diets than other diets.  Much of the reason for this (expanded below) is that when you become insulin resistant then a lower fat diet will provoke high insulin which only adds to the problem. Here is an excellent summary of the 23 RCTs on low carb high fat
  5. More on long term safety – Jim Mann’s main point on the stuff.co.nz article and media release about low carb high fat was around long term efficacy and safety. He does have a point – you can study this through RCTs, but the long term epidemiology isn’t there for eating actual whole plants and animals (short of the work on healthy indigenous populations, and that this is the sort of diet humans have eaten for 99.9% of the time they have been on the planet). There is certainly no evidence of harm – some people like to quote the Swedish women’s study to show there is harm of a high fat, high protein diet. I am not promoting this combination of eating. The epidemiology in this study is woeful because the lowest decile of population carb eaters was still getting 40 percent of their calories from carbs who also had to be in the highest decile of protein eaters – again not what I suggest – had poorer health outcomes.  Again if the cardio- metabolic risk factors are worth anything – then people do better.  Here’s a good dissection of this Swedish paper.

     I think this shows how epidemiology sometimes gives us what we want to see.  I agree that more work needs to be done.  My starting hypothesis is to look at human nutrition through an evolutionary biology lens – what food environments are humans adapted to? And what is the physiology around this?   I think we have to understand how and why insulin resistance happens and how that relates to chronic disease through inflammatory processes. I particularly recommend to you this paper which has a brilliant and comprehensive take on the evolutionary nutritional biochemistry and chronic disease development.  BTW – the 40% CHO diet and high protein combination in the Swedish study showing the highest CVD is very much the type of mix Professor Mann has advocated (to me at least) he would support.

  6. Some longer-term data on Type 1 diabetics and low carb high fat diets – good efficacy and safety.
  7. Mechanistically high SFA doesn’t translate to high plasma SFA in the context of low carb diets – see reference.
  8. I agree that people respond differently to different diets. Insulin resistance is important as to what diet we can tolerate.  Hyperinsulinaemia induces the direct and indirect effects for the major chronic diseases.  Impaired glucose tolerance doesn’t catch this until end stage.  Many many people get glucose into their cells at the right rate, but with hyperinsulinaemia.  Complex carbs may not help, and in fact be even worse because the carbs are digested slowly provoking longer hyperinsulinaemia – a reference. We will publish our analysis of this soon. But in the meantime see the work of Dr Joseph Kraft.
  9. The only way to diagnose this is a dynamic glucose tolerance test measuring insulin.  We have a database of 15,000 of these with insulin for up to five hours post OGTT. You will see the pattern of hyperinsulinaemia with normal glucose tolerance decades before impaired glucose tolerance.
  10. I contend that virtually every CVD risk factor either causes insulin resistance through inflammatory or other processes e.g. Sleep, stress, sugar, alcohol, smoking, pollution and so on.  Obviously some have other effects too (e.g. smoking). But also that age and ethnicity affect Insulin sensitivity – Maori and Pacific are likely to be more prone to the above.
  11. Here’s the kicker for me – in terms of health inequalities the current dietary guidelines probably perpetuate health inequities because the least at risk do the best and stay healthy. So even if the two types of dietary guidance are efficacious – which they are – albeit not equally distributed in their efficacy AND there seems to be no evidence of harm from a lower carb high fat – then we have no option but to go the high fat route because of the inequalities – although I acknowledge we need more work to understand this. That’s the reason I am pursuing this.

Extra references to 23 RCTs showing good outcomes for low carb diets compared to other diets. Actual data summarised here very nicely too

1. Foster GD, et al. A randomized trial of a low-carbohydrate diet for obesity. New England Journal of Medicine, 2003.

2. Samaha FF, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. New England Journal of Medicine, 2003.

3. Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. The Journal of Pediatrics, 2003.

4. Brehm BJ, et al. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. The Journal of Clinical Endocrinology & Metabolism, 2003.

5. Aude YW, et al. The national cholesterol education program diet vs a diet lower in carbohydrates and higher in protein and monounsaturated fat. Archives of Internal Medicine, 2004.

6. Yancy WS Jr, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia. Annals of Internal Medicine, 2004.

7. JS Volek, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutrition & Metabolism (London), 2004.

8. Meckling KA, et al. Comparison of a low-fat diet to a low-carbohydrate diet on weight loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. The Journal of Clinical Endocrinology & Metabolism, 2004.

9. Nickols-Richardson SM, et al. Perceived hunger is lower and weight loss is greater in overweight premenopausal women consuming a low-carbohydrate/high-protein vs high-carbohydrate/low-fat diet. Journal of the American Dietetic Association, 2005.

10. Daly ME, et al. Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes. Diabetic Medicine, 2006.

11. McClernon FJ, et al. The effects of a low-carbohydrate ketogenic diet and a low-fat diet on mood, hunger, and other self-reported symptoms. Obesity (Silver Spring), 2007.

12. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study. The Journal of The American Medical Association, 2007.

13. Halyburton AK, et al. Low- and high-carbohydrate weight-loss diets have similar effects on mood but not cognitive performance. American Journal of Clinical Nutrition, 2007.

14. Dyson PA, et al. A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects. Diabetic Medicine, 2007.

15. Westman EC, et al. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutrition & Metabolism (London), 2008.

16. Shai I, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. New England Journal of Medicine, 2008.

17. Keogh JB, et al. Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity. American Journal of Clinical Nutrition, 2008.

18. Tay J, et al. Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. Journal of The American College of Cardiology, 2008.

19. Volek JS, et al. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids, 2009.

20. Brinkworth GD, et al. Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 months. American Journal of Clinical Nutrition, 2009.

21. Hernandez, et al. Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet. American Journal of Clinical Nutrition, 2010.

22. Krebs NF, et al. Efficacy and safety of a high protein, low carbohydrate diet for weight loss in severely obese adolescents. Journal of Pediatrics, 2010.

23. Guldbrand, et al. In type 2 diabetes, randomization to advice to follow a low-carbohydrate diet transiently improves glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss. Diabetologia, 2012.

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

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

Here are a few of these questions:

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

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

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

“How does a low carb approach change things?”

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

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

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

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

Low carb high fat lecture full, so we are doing another

NEW DATE due to popular demand 22 October

Thanks to the many who have registered and shown interest in this seminar at AUT Millennium on October 16th.  Its been wildly over subscribed to the point we have decided to do a second seminar.  So please if you are interested, its filling very fast, get registered today.

Event Details
Date:   Tuesday, 22 October 2013
Time:   7.00pm – 8.30pm
Venue: AUT Millennium Institute, 17 Antares Place, Mairangi Bay, Auckland

Free public parking is available

Programme

6.00pm – 6.50pm       Registrations open
7.00pm – 7.45pm       Event commences.  Keynote presentation from Professor Grant Schofield
7.45pm – 8.30pm       Q&A session and open discussion followed by refreshments

Note, we will also be taking registrations on the night for a series of corresponding paid workshops that will be held in November. Details about the workshops will be posted on this site once confirmed.

RSVP to attend the event by providing your name, email, and contact number REGISTER

For those international and out of town, we will video and make available online.

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.

Joseph Kraft: Why hyperinsulinemia matters

Joseph Kraft MD
Dr Joseph Kraft MD, pathologist and author of “Diabetes Epidemic and You” and unsung pioneer in insulin responses and early diagnosis of diabetes

Science has a history of ignoring some of the most important and astonishing work for a long time, then coming to its senses and celebrating it. It is time now to celebrate the work of Dr Joseph Kraft MD, a pathologist now in his nineties. Dr Kraft is the author of “Diabetes Epidemic and You” which is still available, at least in hard copy. He defines what he calls “Diabetes in situ” which is borrowed from his cancer pathology background. He has written several good papers, none of which have ended up being cited that highly.  A nice, free summary of his work is available here. Kraft has carried out more than 14,000 oral glucose tolerance tests over a few decades. Normally we measure the glucose response to drinking glucose.  This response can tell us the degree to which we metabolize and remove glucose from our blood.  Very important for diabetes diagnosis and other metabolic issues. Kraft’s test are different though.  He is way more thorough than normal.  First, rather than monitoring glucose for 2 hours post test, he monitors it for at least 5 hours.  Second, he also measures insulin, as well as glucose, over the course of the test. From his test results and the other literature, as well as his pathology and direct autopsy observations, he concludes that:

  1. We may be able to diagnose diabetes much much earlier than we do
  2. Abnormal insulin levels (high) are directly and indirectly damaging to the vascular system, and therefore almost every organ in the body
  3. This high insulin (hyperinsulinemia) is a condition in its own right and really the causal mechanism behind most of the metabolic and chronic diseases we experience today.

He calls the abnormal insulin response, with normal glucose response “Diabetes In SituWhat is Diabetes In Situ? Here’s the deal – you go to your doctor.  You get a series of tests to see how well you are functioning metabolically. This is a really important series of tests because metabolic functioning is what will determine almost all of our quantity and quality of life. I would go as far as to at least hypothesize (there’s enough evidence) that problems in carbohydrate metabolism are implicated in virtually every chronic disease from head to foot, and most of the organs in between.  This includes Alzheimer’s and vascular dementia, peripheral vascular disease and everything in between, from common obesity to diabetes to fatty liver disease to cardiovascular disease…and the list goes on. The trouble is that your doctor will look for metabolic markers which are either flawed as predictors, or mostly are markers of end stage dysfunction. Things like elevated blood glucose, high blood pressure, vascular blockages (arterial sclerosis) etc. If your doctor is really interested in your health and suspects you aren’t doing that well, they might order an oral glucose tolerance test. Kraft shows us that there are five typical patterns of insulin response to the glucose which characterize disease state.  As mentioned earlier, these are really what we should be considering in early identification of metabolic problems. Unfortunately, the glucose tolerance test is rarely run long enough, nor is insulin (key to this) measured concurrently.  In fact, in New Zealand, insulin measurement can only be ordered and covered under the public hospital system by a handful of specialist endocrinologists. Insulin is not considered as useful in the diagnosis of early stage chronic disease. That’s a shame really because Dr Kraft shows it certainly is useful. Let’s look at Kraft’s five patterns….. Here’s what we consider a normal insulin response to a glucose bolus in an oral glucose tolerance test. Kraft calls this “Pattern 1”. Pattern 1 insulin peaks after a 75 or 100 g glucose load after 30 to 60 min at 50-70 units. Everything is almost back to baseline after 2 hours, certainly after 3 hours. This is what we regard as a normal insulin response to a glucose load. It’s also likely that slower release carbs (lower GI) like beans might provoke an even lower area under the curve for the same total CHO load. Pattern 1

Pattern 2 (below) is the first sign of insulin resistance, but things will likely look fine if you simply look at the glucose responses. We see a similar time to peak, but a much higher peak. Insulin hasn’t returned to close to baseline until 4 hours or so after the initial load.  The area under the insulin curve is very large.  The total stress on pancreatic beta cells is high simply because of the overall demand for insulin. Many (most) people with this pattern present normal glucose curves and are told they are doing “just fine”.

Pattern 2

Pattern 3 (below) is a delayed and high peak.  This is indicative of some beta cell function, but some functional loss.  In essence we are seeing the beginning of beta cell burn out.  People can eventually move glucose into their cells, but they take a long time to produce enough insulin.

Pattern 3

Pattern 4 (below) is the same as Pattern 3 except the fasting level of insulin is much higher.

Pattern 4

Pattern 5 (below) is beta cell failure. In other words, there is little or no ability to move the glucose into cells because the pancreas can’t produce insulin. Patients will need exogenous insulin injected at that point to get the same result. Interestingly, Kraft also shows that sometimes people on low carb diets can show this pattern temporarily. It’s not that they are unable to produce insulin, it’s just more likely that they can take up glucose into cells (eg, brain) without insulin in the first instance.  These people return to Pattern 1 after a period on a higher carb diet. I think this is also consistent with the finding that people on LCHF diets typically have a temporary diagnosis of peripheral insulin resistance which is resolved after a large carb meal. It’s likely that the body adapts to preferentially shunt the available glucose to the brain first.  So Pattern 5 with a low carb diet is OK, its jus the same physiology as Pattern 1 but adapted to low carb. Pattern 5

Take-home messages, implications for practice, and questions

  • Dr Kraft was onto it decades ago – that we should measure glucose and insulin concurrently for an extended period in the glucose tolerance test to identify those people who are at risk early.
  • This early detection is both ethical and necessary.
  • Instead current best practice sends people away who are insulin resistant until they present with end stage disease markers.  Only then will we take them seriously.
  • Why haven’t we taken Dr Kraft’s excellent work more seriously?

Finally here is a link to a letter I received from Dr Kraft recently. He outlines is overall approach and ideas from his results of several thousand OGTTs over several decades.  It’s interesting stuff – page 1 click herepage 2 click here

As usual, for all my blog thanks so much to Helen Kilding who tirelessly edits and corrects my terrible typing!

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.