Some fun media with me….A public health professor believes New Zealand schools should run lunch programmes to reduce the consumption of processed and packaged food.
Listen to the interview (4 min and fun – tight here): Schools encouraged to run lunch programmes to promote healthy eating
Dr Richard Babor, a cancer surgeon, and his new TV show “How not to get cancer” attracted loads of attention. There was some negative reaction because people felt they were being unfairly blamed for getting cancer, because poor lifestyle was pinned as a major cause of cancer. I doubt that was the intention of the show. In fact, Dr Babor clearly started in the intro that “it’s no one’s fault personally” and this is an important point.
But it is a big public health issue. No one wants cancer, and we want to know if we can prevent it.
The way public health researchers have assessed the situation is to look at cohorts who behave in certain ways and those who do things differently. What we have seen is that things like smoking, poor diet, low fitness and activity, poor sleep and other lifestyle factors account for quite big differences. Maybe half of all cancers could be prevented by healthy lifestyle.
That’s not a personal fault of anyone. But it is a big societal issue. I’m assuming we all want along and healthy life.
We’ve grabbed smoking by the horns over the last few decades. Drinking is improving in some groups. Food guidelines and the food environment have been hijacked by the processed food industry. Fitness continues to plummet, especially in our kids.
This post is about fitness.
It’s about how some of the finer details which can make a big difference.
It includes the extra information that didn’t fit into the few minutes of my appearance on Dr Babor’s show. I’ve been asked a lot to write about this and provide some detail and “how to” of what he did and how he massively helped his fitness by slowing down, doing a little less (but still plenty) and boosting the physiology of the anti-cancer environment.
It’s about the finer details that are important for our long-term health and happiness. I’m assign there are a lot of people who want the best actable information about lifestyle and health, not the “minimum guidelines for couch potatoes”.
Fitness is medicine. So here goes….
The features of the pro- and anti-cancer internal environment
One way of thinking about human physiology around growth and repair cycles is to understand the catabolic versus anabolic states. In catabolism your body is repairing and tidying up what it has – it’s a non-growth, use-what-you-have state. In anabolism, you are growing more – cells divide – you grow, you store.
One view is that most modern humans end up spending far too much time in the anabolic (growth and storage) state, and not much time in the catabolic (repair and use) state. Because the anabolic state is one of inflammation – that’s what stimulates the process, then this chronic inflammation is never stopped and this is the root cause of modern chronic disease – cancer, heart disease and stroke, Alzheimer’s disease and dementia, and diabetes.
One way the catabolic environment might deal with early cancer cells is that they (early cancer cells) are metabolically disadvantaged in this state. Cancer cells themselves are unable to become catabolic. Early cancer and pre-cancer cells may be more likely to be recycled through autophagnic and apoptotic processes. The anabolic state is pro-cancer because it is a growth-promoting environment – exactly what early cancer cells want. The inflammation and reactive oxygen species might create further mutations to more aggressive cancer type cells.
There’s some speculation above, but I think the evidence points the fact that we could do with getting into the catabolic state from time to time. Regularly even.
The features of a catabolic state (cell repair, use of whats left, stimulated by nutrient stress)
- Low insulin and glucose
- Low IGF-1 (insulin-like growth factor)
- Low reactive oxygen species
- Ketogenic signalling
- High immune functioning
The features of an anabolic state (cell growth, storage, stimulated by food and stress)
- High reactive oxygen species
- High IGF-1
To be clear both states are essential for fully functioning healthy humans. But you do need to be able to access both.
What we need to get catabolic signalling going is nutrient stress. That is, not enough nutrients. This forces the body to stop the growth and scavenge through a process called autophagy (literally self eating) where every cell in the body uses the lysosome to recycle and find old organelles and scraps floating around inter- and even extra-cellularly.
It’s a process essential for optimal function, including probably the early destruction of cancer and pre-cancerous cells (see above).
Fasting (i.e. not eating) is the most obvious way of stimulating catabolism. Getting insulin higher (eating carbohydrate and protein) is the path to anabolism.
Fasting and fasting mimicking
Here are the known ways to get that catabolic environment. It turns out you can get the same (or similar) effects to fasting while still eating as well!
- Extended fasting. That’s right – not eating for a few days gets you right there. I’ve done this several times and you feel great. But it does have some drawbacks…Pros: Save money, get ketogenic signalling going quickly. Cons: You are not eating, people classify you as “that person”, and you may lose muscle mass and reduce your metabolic rate.
- Intermittent fasting. Not eating for longish periods during a day e.g. miss breakfast and lunch. I’ve done lots of this and wrote a book (What the Fast?) all about this. I find it a practical way to cycle in handout of the catabolic state. Pros: Pretty simple, save money, you have more time during the day to do other things. Cons: Still requires will power.
- A fasting mimicking diet (keto). I written even more about this in all the What the Fat? books. I like low carb as a base for living. Pros: It’s yummy, you feel full, you get the nutrients you need. Cons: It can be costly, takes preparation, and sometimes you feel a little limited in the pathological food world we live in.
- Fasting mimicking Exercise (FME). I’ve written almost nothing about this and it’s about time I did, because exercise training on a healthy diet where the intensity is low (at or below aerobic threshold) has a profoundly useful signalling effect on the body – it stimulates low glucose, insulin, IGF-1, increased ketones, and all the rest of the catabolic pathway. That’s why I’m calling it FME. Pros: It’s free, it’s fun, it’s super easy (the effort level is ridiculously and counterintuitively low), and you get the benefits like increased cardiorespiratory fitness (see below), relief of arthritis and back pain, better mood and mental health, and increase muscle mass and your metabolic rate. Cons: You have to do it, but even when you don’t feel like doing it, you return feeling like it was worth it.
So there is your quiver of catabolic tools. Most of you would have heard of the first three. Here’s to adding the fourth, FME!
Oh, but wait there’s more. Being fit is good for you for lots of reasons. Here’s some epidemiology.
Why fitness is medicine
It’s long been known that high fitness is associated with better health – living longer and with less disability. But there has always been a thought in public health that we may as well just tell the half of us who hardly move at all (or don’t meet the minimum physical activity guidelines) that any movement is good movement, and that 30 min of anything 5 days a week is enough.
True, it’s enough for the minimum benefit. You are way better off doing something than nothing. So if that’s you, read no further and go outside and get started.
There has also been a school of thought that we have people in society who take their fitness way too seriously. We even give them names like “fitness freak”. (I’ve been called that…)
I submit to you that there are many in society who want to have the full information about what constitutes optimal health and best possible outcomes. This is what this post is about in regards to fitness.
I guess the idea that you can wreak havoc by overdoing it is real. I have over-trained, and achieved less than optimal fitness by being an idiot about it. Hopefully I can show you the best way to not get into this space.
What recent studies have shown us is that there is no such thing as “too fit”. The fitter you are the better you do on pretty much everything.
Here are a couple of studies to show you this.
First, this study in the Journal of American College of Cardiology shows a linear dose-response between fitness and all cause death, cancer death, and cardiovascular death. The least fit are twice as like to get all of these.
An important feature is the continuous dose-response relationship.
In the paper “Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing” they followed more than 122 000 people for more than 8 years. what was cool here was that they had enough people in the study to look at the very fit ones. The top few percent they called “elite fit” older adults.
Here’s what they found:
Results The study population included 122 007 patients (mean [SD] age, 53.4 [12.6] years; 72 173 [59.2%] male). Death occurred in 13 637 patients during 1.1 million person-years of observation. Risk-adjusted all-cause mortality was inversely proportional to cardiorespiratory fitness and was lowest in elite performers (elite vs low: adjusted hazard ratio [HR], 0.20; 95% CI, 0.16-0.24; P < .001; elite vs high: adjusted HR, 0.77; 95% CI, 0.63-0.95; P = .02). The increase in all-cause mortality associated with reduced cardiorespiratory fitness (low vs elite: adjusted HR, 5.04; 95% CI, 4.10-6.20; P < .001; below average vs above average: adjusted HR, 1.41; 95% CI, 1.34-1.49; P < .001) was comparable to or greater than traditional clinical risk factors (coronary artery disease: adjusted HR, 1.29; 95% CI, 1.24-1.35; P < .001; smoking: adjusted HR, 1.41; 95% CI, 1.36-1.46; P < .001; diabetes: adjusted HR, 1.40; 95% CI, 1.34-1.46; P < .001). In subgroup analysis, the benefit of elite over high performance was present in patients 70 years or older (adjusted HR, 0.71; 95% CI, 0.52-0.98; P = .04) and patients with hypertension (adjusted HR, 0.70; 95% CI, 0.50-0.99; P = .05). Extreme cardiorespiratory fitness (≥2 SDs above the mean for age and sex) was associated with the lowest risk-adjusted all-cause mortality compared with all other performance groups.
In actual plain English this means that
- The fitter you were the better
- The elite fit had 5 X less chance of dying than the least fit people.
- This effect is akin to the effects of smoking
- There is still a large effect even from moving from the high fit to the elite fit group
Yes it’s a prospective study. There may be confounders, but it’s unlikely with the effect sizes this large and the known biology involved. In my opinion, the totality of the evidence easily meets Sir Austin Bradford-Hill’s criteria for causal inference.
Why exercise works – exercise physiology
Just as an important note, I think we should do a bit of exercise physiology. First is the concept of Hormesis. Hormesis is the theory that sub-toxic stress is good if we can adapt to it. We end up adjusting our biology to cope with that stress.
We rebuild bigger faster, stronger, more resilient to that stress.
Lose dose radiation is good for us, the toxins in plants may be good for us, cycling between heat and cold stresses in a sauna is good for us, and exercise if we adapt is a stress which can produce a resilient,. stronger system, What doesn’t kill us makes us stronger right?
All good so far. But I think we should be thinking about exercise in two separate stressful modes. They are stressful for completely different reasons.
The first I’ll call anabolic exercise. It’s short and high intensity. You burn glucose and you damage the cells in the body. They respond. This is why weight training, HIT (high intensity interval) training are important and useful. It’s also why you shouldn’t over do this, and should periodise your exercise and allow recovery between hard efforts. It’s my view that many exercisers do too much anabolic exercise and do not allow enough recovery. The damage you create is inflammatory and acutely is good for you. Chronically it’s bad. This is what leads to burnout, sickness, and injury.
What we hardly talk about is catabolic exercise. It’s typically very easy aerobic exercise that creates stress through nutrient stress pathways. That’s why I call it Fasting Mimicking Exercise. It reduces glucose, insulin, IGF-1, inflammation, improves immune function, and generates ketogenic signalling pathways.
Both types of exercise are stressful. Both have hormetic effects. Both are useful.
If you want to exercise catabolically, then you need to know about the Maximum Aerobic Function or MAF.
MAF is where you move from exclusive use of the aerobic energy system to include the increasing use of the anaerobic system. Exercise below this level is easy, feels easy – even if you are unfit – you will just go slower the less fit you are. in practical terms it’s where you have any hint of puffing at all. It’s a pace you could carry on with indefinitely. It’s my view that most exercisers don’t go easy enough to achieve this level.
MAF shouldn’t confused with the anaerobic threshold which is what you sustain in a very hard 30-60 min of intense exercise and above this you can’t speak at all. We are not aiming for this level of hard. In fact, most of us should avoid this except for the occasional high intensity interval training. Its my view that this is where most people exercise when they exercise. No wonder they are tired and find motivation an issue.
I first heard about MAF from Mark Allen (6 time Hawaii Ironman winner) in 1995 at a pro race briefing at the Hawaii Ironman triathlon world championships. I was also a pro athlete there and thought that I may as well ask him what he did to be so awesome.
He was surprisingly forthcoming. He told me about the methods of his coach Dr Phil Maffetone. Allen trained with a heart rate monitor. He did most of his work at or under his MAF threshold. The MAF heart rate is simply:
MAF heart rate = 180 – age
- Add 5-10 beats for high lifetime fitness and being fit
- Subtract 5-10 for sickness, low fitness
Exampleme (Grant, aged 50) = 180-50 = 130 add 10 beats for lifetime experience and high fitness = 140
Example (38 year old female, not very fit) = 180-38 = 142 low fitness = 138
Allen explained that this give him all the fat burning and fitness benefits he needed to be the old champion without all the inflammation and burnout, injuries and tiredness others got. He further explained that Dr Maffetone insisted he maintain a low carb high fat diet to further the process, because high carb, sugar diets made it harder to get the catabolic fat burning benefits from the MAF training.
That was interesting, and completely contrary to what I (a trained scientist) knew about exercise training and nutrition. Remember, I was in the land of Gatorade and threshold training.
So I flipped off his advice as lies and propaganda and keep drinking Gatorade and eating pasta and trained as hard as I could. I got inflamed, sick and fat. Allen went on to win another title!
It was another 17 years before I came to understanding the genius of Maffetone. He was miles ahead of us. Decades later!
Read more about Dr Phil Maffetone here
The MAF test
Now comes the key to this, and what I did with Dr Babor among others. Monitoring your fitness progress using the MAF test is a critical factor in understanding if your exercise is working the way it should. If you exercise and you aren’t getting fitter then what are you doing?
You can read much more on Dr Maffetone’s MAF test on www site here
Maffetone has you walk, jog, or run (depending on your fitness) at your MAF heart rate for 5 miles measuring the time it takes to do each mile. It’s super easy because you are at such a low heat rate, so the test itself hardly feels like a test.
Here are the improvements in MAF test results of a marathon runner over several months. It’s impressive stuff.
The test monitors your progress. The MAF pace training improves you without the stress and risk of hard exercise.
OK, well we are not all marathon runners so let’s move down some levels. First here’s me over a two-month period doing a Thursday run. I opted not to do the 5 X 1 mile test, but just went to a hour or so run-walk on the same circuit. I had a break between lectures on Thursday so went out to get some space. The run was up and down hills and off road in places. I had to walk almost all of the hills to stay under 140 HR.
You will see I improved using MAF training by an incredible 11 min over two months. In other words, I ran the same circuit with the same heart rate 15 percent faster just doing easy jogging and walking. This translates into faster paced running too. I cracked out a 1.25 hr half marathon just doing this. I had been trying prior to this, and too hard. I was only able to run a 1.34 half marathon despite harder training before this.
|Weekly run (hilly bush loop form AUT Akoranga campus around Tuff’sCarter and through Kauri Glen bush)||Run time
@ <140 BPM
|1st March||72 min|
|8th March||69 min|
|6th April||62 min|
|13th April||64 min|
|20th April||62 min|
|27th April||61 min|
In the “How not to get cancer” show I prescribed Dr Babor a MAF exercise program based on fasting mimicking excess principles. I adapted Phil Maffetone’s “MAF” test but used kilometres. It takes less time and yields just as much information. And In my part of the world, who knows what a mile is anyway. A km is way easier to figure out, and it’s how we measure pace when we run/walk
His results astonished even me. In test one on the running track outside my office here at AUT Millennium he managed about 8.30 min per km. That’s pretty pedestrian.
This surprised me because he was going for 90 min hard runs and feel quite tired for his exercise.
Over the next four months he did a similar or slightly less volume, and kept his heart rate under his MAF threshold. He used a heart rate monitor to do so. This meant walking up lots of hills.
Look at the improvement (some due to learning to do the test better perhaps) but he was running 3 min/km faster for the exact same heart rate!
All this by slowing down, and getting catabolic.
As Mark Allen told me. I think this works better when augmented with a low carb diet. That’s the ultimate fasting mimicking, catabolic way to live and therefore the “anti-cancer” combination Dr Babor was looking for in his show.
|Kilometre||Test 1 July 8th
@ <134 BPM
|Test 2 Oct 23rd
@ <134 BPM
Matt Kerr: High performance
I wanted to finish with an actual high performance example. This is Matt Kerr, whom I coach. He’s an elite triathlete. He’s lean, he’s fit, he’s fast.
But he was training too hard, and eating too may carbs in my opinion.
We tested him on our more advanced equipment at our Human Performance labsat AUT Millennium. You get a lot of information about fat burning, catabolic and anabolic exercise, and pace with this sort of testing.
Here’s Matt’s metabolic flexibility curve at high carb, high intensity training at baseline. Remember he is extremely fit. He’s just come off some good shorter racing. But he’s a carb burner. He hardly ever burns fat, and doesn’t do that very well.
Although fit, he had a series of winter injuries I think related to poor training and diet.
He was maxing out at 0.52 g/min of fat burning and doing so at 135 w of power on the bike. That’s slow. That means he relies on carb burning. It means that almost all of the 20 hours training a week he does creates an inflammatory, low immune function, high ROS environment. That’s a recipe for sickness, injury and poor performance especially in long races.
I threw Matt onto a keto diet, MAF train for almost all of his sessions, and included some fasted long rides at a very easy pace.
He could now oxidise 1.1 g/min of fat and could do so at 240 W on the bike. That’s fast and it means training and racing is a clean burning low inflammation, low ROS, high immune function environment
He ended up placing in the top 10 at Ironman NZ in his first race over that distance, in 9 hr 18 min.
OK, this won’t mean much to most of you. For those in that game, its an incredible result. The results for myself, Dr Babor, and Matt show that the same principles apply across all sorts of individuals. I’ve used this with young and old, fast and slow with the same results.
You see, we are all human and we will respond to the stress of catabolic FME. You can’t fail with this if executed properly.
Tools you will need
(disclosures – I have no association with any of these products or companies other than I have bought them and use them myself)
There is just no way around this. If you want to do this method you need an objective measure of effort and heart rate is the easiest. You will need a heart rate monitor of some sort. My preference is an actual smart watch with wrist-based HR. Here’s my Garmin 235 which is the cheaper, but still expensive….
Well there is a way around it. If you can’t afford a heart-rate monitor, just measure the rate by taking your pulse with a watch after different types of exercise to get some idea where your MAF range lies. Believe me its hard to get that really to the level of accuracy you need, but possible I guess.
My watch downloads to a smart app. It’s fun and easy to use.
You can also connect to Strava – a sort of social media for fitness. Its really fun. I have all my friends and family on it. OK, not for everyone but it is cool. Your friends can give you “kudos” which sounds corny but is great.
I also bike lots, swim and surf a bit, and walk a lot. All of these pop up on my smart watch and Strava. Here’s yesterday’s bike in the trainer (I use Zwift, a game type program which is also heaps of fun – you can see my setup in the video at the end of this post).
OK you don’t need to have all the tech stuff I do. But I do love this stuff and it’s a great investment, if you can afford it, in your health and well-being.
How much money do we spend on sickness in our society?
We should dish this stuff out at the doctor. Imagine you go to the doctor and come back with a Garmin 235, a bike, a smart trainer and a Strava account!!
Probably we would save the country money and improve our lot as a society?
Practicalities and final words
Society needs a new perspective on fitness. We need to take it regularly, seriously, but not too hard.
Let’s give up on the term, fitness freak!
If you are going to go this way then get others involved otherwise you’ll be so slow they’ll leave you behind while they all rush off into inflammatory, anabolic exercise land. You have to get your head around the fact that this is slow and easy, and that counterintuitively you get the real benefit by slowing down.
You want the whole peak performance – to be the best you can be – so yes, do the weights and high intensity as well, but not too much.
How much volume is too much? That totally depends on where you are starting from. But very fit humans can easily manage a few hours (or more) of MAF./FME a day. You don’t have to do that unless you are in training for an Ironman triathlon or similar. So start with what feels easy and take it from there. Just keep the heart rate down. Walk when you need to, and leave your ego in a brown paper bag on the kitchen bench before you go out the door. You can collect it when you get back.
I’ll leave you with my short video on “fitness is medicine” (watch out for Bluey, my border collie who is the main star) – enjoy and see you out there (going slowly!)
The other day a new paper modelling a saturated fat tax came out in the journal PlosOne.
In order to improve the population’s diet, the World Health Organization has called for the taxation of foods that are high in SFA.
Oh no not this again! There are very strong socio-economic reasons why such a tax makes no sense, and would probably have the opposite effect of a sugar tax, but before we get to discussing that we’ll look at what the authors did, what they got right, and where they went wrong.
First up, they (all 3 authors are public health analysts, none has published an experiment) are modelling the predicted effect of a tax on fat consumption, using data from Denmark, which had a short-lived saturated fat tax. it was a stupid move for two reasons. First, higher LDL cholesterol is associated with longevity in Denmark – you’ll see how they missed this next. And second, the revulsion against the saturated fat tax and its effect on traditional foods saw both the fat tax and Denmark’s longer-lived sugar tax being thrown out at the next election. So this folly cost them any benefits of their sugar tax. Then, they are modelling the expected rate of CVD (heart attack and stroke) mortality from the predicted changes in LDL cholesterol from substituting polyunsaturated fats (PUFA) for saturated fats (SFA), based on feeding studies.
But hang on – what about the odds of dying from other conditions, like cancer, diabetes, etc? This – all-cause mortality – is not mentioned at all. For all we know we’re shifting the disease burden around, or making it worse overall. Or there may be no benefit for CVD at all either (see admissions below).
The authors get a couple of things right. They acknowledge that there’s no evidence that SFA, by itself, is associated with CVD. Then they turn to the type of computerised remodelling of epidemiological data invented about 10 years ago that looks at replacing one fat with another. In this, it usually (but not always) looks as if replacing SFA with PUFA lowers CVD risk. That’s a hypothesis – so has anyone tested the hypothesis?
Yes they have – and to their credit these authors cite Steve Hamley’s meta-analysis, which corrects errors of data extraction found in others and discusses the confounders in various studies.
A recent meta-analysis, which based their findings on randomised controlled trials, concluded that replacing SFA with PUFA would have no effect on major IHD events . Nevertheless, it is argued that prospective cohort studies find the replacement of SFA with PUFA to be beneficial for the prevention of IHD.
Um, this is epidemiology in reverse. RCTs are the opportunity to test the hypothesis. The Cochrane Collaboration recently summarised the RCT evidence thus, in substantial agreement with Hamley: So are we really to base such big public health changes on no real data of efficacy and a simple hypothesis? How did that end last time with the low fat revolution?
Increasing PUFA probably makes little or no difference (neither benefit nor harm) to our risk of death (moderate-quality evidence), and may make little or no difference to our risk of dying from cardiovascular disease (low-quality evidence). However, increasing PUFA probably slightly reduces our risk of heart disease events and of combined heart and stroke events (moderate-quality evidence). Fifty three people would need to eat more PUFA to prevent one person experiencing a heart disease event, and 63 people to prevent one person experiencing a heart or stroke event. Increasing PUFA may very slightly reduce risk of death due to heart disease, as well as stroke, but harm is possible (low-quality evidence). PUFA probably slightly reduces fats circulating in the blood (triglycerides, moderate-quality evidence but without effects on other lipids or adiposity). The evidence mainly comes from dietary-advice trials of men living in high-income countries.
There’s a very important point here – although PUFA lowers LDL-cholesterol in the short term feeding studies that the tax modelling paper relies on, Cochrane haven’t highlighted that effect in the RCTs. Recently we looked at a study co-authored by Jim Mann where Chinese subjects were fed 40% of calories as soybean oil for a year – a very high PUFA intake. Did that lower their LDL? At the end of the year they had changes to their gut bacteria that Mann thought compatible with an increased risk for bowel cancer and heart disease – but their LDL cholesterol was the same, and they had higher triglycerides.
“The high fat group had a very different profile of bacteria in their gut, one more compatible with an increased risk of bowel cancer and also a much higher risk of inflammation leading to cardiovascular disease, heart disease and possibly diabetes,” Prof Mann says.
So we see that increasing PUFA in real life, which is the intended effect of the tax (or the only way its authors think it might benefit us) does not always produce the results they are predicting from short-term feeding studies done in healthy young white male subjects.
The feeding studies are interesting because they show that some saturated fats (lauric and myristic acids) raise LDL much more than other SFAs. So if the SFA -> LDL -> CVD hypothesis were true, these fatty acids should be the ones most associated with CVD, right?
But no – in every epidemiological study that separates different fatty acids, the cholesterol-raising SFAs are those least associated with CVD. Sometimes, they have a “protective” association.[6,7,8,9]
So what does this mean? Obviously, the cholesterol-raising effect of SFA does not have the same effect on cardiometabolic risk as the cholesterol-raising effect of the genes for familial hypercholesterolaemia. Why anyone still thinks that it can is beyond comprehension – almost every pathway is being influenced in a different way. Yet this crudest of analogies is what we seem to be stuck with as a replacement for the scientific process.
Harm is possible
Cochrane said of PUFA in the RCTs, “but harm is possible (low-quality evidence)”. What does this harm look like in epidemiology?
An increased risk of severe pre-eclampsia (a condition of high blood pressure and proteinuria in pregnancy which can result in seizures) is associated with higher ALA intake in Denmark (canola oil is the main source of ALA there) – RR 1.71
Note that DHA and EPA (fatty fish) have a protective association with severe pre-eclampsia; saturated fat has a protective association with pre-eclampsia which shows a clear dose-response in minimally adjusted (0.63) and multivariable adjusted (0.73) models, but is non-significant in the most adjusted model. Dairy fat is the main source of SFA in Denmark.
This is the country where they actually imposed a saturated fat tax, remember? It’s unlikely they did any modelling around complications of pregnancy beforehand.
Increased risk of melanoma and other skin cancers is associated with higher LA intake in the USA. This is in the NHS/HPFS database, where PUFA usually tends to look better than it does in most other cohort studies; the mechanistic explanation laid out in the paper is a strong one.
Higher intake of omega-6 fat was associated with risk of melanoma (pooled multivariate HR, 1.20; 95% CI, 1.02–1.41; Ptrend=0.03) although the association was attenuated and no longer significant after adjusting for other types of fat simultaneously.
For SCC [squamous cell carcinoma], although total fat intake was not associated with the risk, polyunsaturated fat intake was associated with SCC risk (pooled multivariate HR, 1.16; 95% CI, 1.05–1.28; Ptrend=0.001) (Table 3). Among types of polyunsaturated fat, higher intake of omega-6 fat was associated with SCC risk [HR, 1.23 (1.08, 1.41)]. We also found that cholesterol intake was associated with lower risk of SCC.
Similar associations were also seen for basal cell carcinoma. Co-incidentally or not, the skin cancer death rate in NZ doubled soon after margarine was “legalised” in 1972 and has not declined since despite the slip-slop-slap campaigns and introduction of high-SPF sunscreens. And this is a serious problem, because avoiding sunlight is associated with increased CVD risk – another unintended consequence that modelling will overlook.
How does this compare with a tax on sugary drinks?
The proposed saturated fat tax is not just a different version of a sugar tax, but its opposite. We support a tax on sugary drinks because it targets an unfair price difference – Coca Cola is cheaper than “healthy” alternatives like bottled water, and this price point difference drives people, especially those with less money, towards the drink that will cost them more in the long run. A tax on sugar content goes a small way towards correcting this imbalance. Despite the small extra “penalty” cost to those poor people who still drink SSBs, which some understandably object to, it will tend to make their habits a little more like those of the rich.
The proposed saturated fat tax will do the opposite. Highly saturated fats like coconut oil, butter, and beef and lamb dripping are already about 4x as expensive as the refined seed oils that are high in PUFA. This makes them foods of the healthier, better-off classes. This pricing difference already drives disadvantaged people towards seed oils and the foods made with them – KFC (chicken, higher in PUFA, is also cheaper than other meats), Best Foods mayonnaise, and margarine. If these high-PUFA foods were truly healthier, these populations would be better off as a result – but this is so, so not the case. A saturated fat tax just puts real foods and healthy fats (remember, dairy fat and coconut oil are not even associated with increased disease risk) further out of reach of the poor. It increases the gap between the dietary habits of the rich and poor.
At the very bottom of their paper, the saturated fat tax authors admit that the Danish saturated fat tax (20% on the price of butter etc.) was counter-productive, even according to their own logic.
Finally, a fundamental assumption in our study was that PUFA intake would increase accordingly. This assumption is in line with the dietary recommendations that SFA should be replaced with PUFA [21, 53], and other modelling studies that have assumed the SFA reduction would be replaced by PUFA [14, 16, 17, 20] (see S1 Table). A SFA decrease without a simultaneous increase in PUFA does not seem to be beneficial for health [55, 56]. In Denmark, the decreased SFA intake (ranging from 1.6% in males above age 85 to 4.9% in females aged 55–69) seems to have been accompanied by a changed PUFA intake ranging from a 3.1% decrease in males above age 85 to a 0.3% increase in females aged 60–74 . Therefore, our assumption may lead to an overestimation of the health benefits. Foods contain a mix of SFA, MUFA and PUFA. Therefore, further research needs to examine how this corresponding substitution of PUFA can be assured, rather than a replacement by MUFA or carbohydrates. For instance, a price increase for products high in SFA might need to be coupled with a corresponding price decrease for products high in PUFA.
(If you lowered the price of soybean oil any more you’d be giving it away for free, but OK, whatever you say). Despite this awareness, they still went ahead and published a paper claiming via computerized projections that a saturated fat tax would prevent CVD deaths, even though they had evidence the tax as applied in its only real-life example hadn’t worked as designed (even if you don’t factor in the extinction of the sugar tax it caused). Meanwhile, across the bridge in Sweden an increase in butter consumption, with a drop in carbohydrate intake, has coincided with a halving of the heart attack death rate over the past 15 years.
We’ve said it before and we’ll say it again – public health analysts need to get out among the people they are trying to protect; they need to shop alongside them for a start. The saturated fat tax authors don’t have a clinical intervention to their name. They have no idea what will work in the real world. You can build all the models you like; you can build the Millennial Falcon, for example, but you are never going to see one fly in real life.
 Substituting polyunsaturated fat for saturated fat: A health impact assessment of a fat tax in seven European countries
Johanna-Katharina Schönbach , Wilma Nusselder, Stefan K. Lhachimi
Published: July 10, 2019https://doi.org/10.1371/journal.pone.0218464
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Effects of dietary fat on gut microbiota and faecal metabolites, and their relationship with cardiometabolic risk factors: a 6-month randomised controlled-feeding trial.
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 Praagman J, de Jonge EAL, Kiefte-de Jong JC et al. Dietary Saturated Fatty Acids and Coronary Heart Disease Risk in a Dutch Middle-Aged and Elderly Population. Arteriosclerosis, Thrombosis, and Vascular Biology. 2016;ATVBAHA.116.307578. https://www.ahajournals.org/doi/10.1161/ATVBAHA.116.307578
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risk of myocardial infarction in a UK and a Danish cohort. International journal of cardiology. 2018;10:064. https://doi.org/10.1016/j.ijcard.2018.10.064
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 Martin Feelisch, Victoria Kolb-Bachofen, Donald Liu, Jon O. Lundberg, Lucia P. Revelo, Christoph V. Suschek, Richard B. Weller, Is sunlight good for our heart?, European Heart Journal, Volume 31, Issue 9, May 2010, Pages 1041–1045, https://doi.org/10.1093/eurheartj/ehq069
By now you’ve seen these headlines. But what can we learn from the study behind them, and the way it was reported?
The UK Biobank study was a prospective epidemiological study, using the following methods to look at several foods and their association with colorectal cancers:
We used Cox-regression models to estimate adjusted hazard ratios for colorectal cancer by dietary factors in the UK Biobank study. Men and women aged 40–69 years at recruitment (2006–10) reported their diet on a short food-frequency questionnaire (n = 475 581). Dietary intakes were re-measured in a large sub-sample (n = 175 402) who completed an online 24-hour dietary assessment during follow-up. Trends in risk across the baseline categories were calculated by assigning re-measured intakes to allow for measurement error and changes in intake over time.
Here’s a sample of the questionnaire that was used. You’ll see that it collects information about many more types of food than appear in the results. We don’t know how the reported foods were chosen – we’ll return to this later with regard to fibre.
What were the results?
During an average of 5.7 years of follow-up, 2609 cases of colorectal cancer occurred. Participants who reported consuming an average of 76 g/day of red and processed meat compared with 21 g/day had a 20% [95% confidence interval (CI): 4–37] higher risk of colorectal cancer. Participants in the highest fifth of intake of fibre from bread and breakfast cereals had a 14% (95% CI: 2–24) lower risk of colorectal cancer. Alcohol was associated with an 8% (95% CI: 4–12) higher risk per 10 g/day higher intake. Fish, poultry, cheese, fruit, vegetables, tea and coffee were not associated with colorectal-cancer risk.
76g doesn’t sound like much, but believe it or not was the highest meat and processed meat category in the results. What’s a 20% increase in terms of absolute risk? Because the risk is reported as HR not RR we can’t be exact, but the absolute risk of CRC in the study over 5.7 years was 0.5%, 20% would raise that to 0.6%, which is an increase in absolute risk of 0.1%, or one extra chance in a thousand.
But that summary doesn’t tell us the full story; there are two interesting details in the paper. The first is placed right at the start – this “results” table usually appears once tables for factors like representivity and the confounders at baseline have been displayed, which is the approved way of showing the strengths and weaknesses of the epidemiological process, but not this time. Zoe Harcombe has pointed out that the red meat associations cross the centreline, that is, they are – as always – not statistically significant. (I don’t remember the authors mentioning that to the press).
The other important fact they didn’t mention appears further down the paper. And I mean right down near the bottom, with the details restricted to the supplementary papers!
Supplementary Table 4, available as Supplementary data at IJE online, shows the main results in men and women separately. There was heterogeneity by sex for the associations between colorectal cancer and red and processed meat (Pheterogeneity = 0.008), with a positive association seen in men [HR for each 50-g/day increment in red-meat intake = 1.39 (1.17–1.64)] and no association was seen in women [HR for each 50-g/day increment in red meat = 0.99 (0.83–1.19)]. There was also heterogeneity by sex for red meat (Pheterogeneity = 0.008) and for processed meat (Pheterogeneity = 0.022). There was also heterogeneity by sex for alcohol, with a positive association seen in men [HR for each 10-g/day increment in alcohol intake = 1.12 (1.08–1.17)] and no association seen in women [HR for each 10-g/day increment = 0.99 (0.93–1.06), Pheterogeneity = 0.002]. There was no heterogeneity by sex for the associations between fish, dairy milk, cheese, fruit, vegetables, fibre, tea or coffee and colorectal cancer.
So of all the associations tested, only fibre from grains (14% lower risk, remember) had any association with colorectal cancer risk in women, or the same risk as seen in men.
We’ve looked at several of the reports on this study in the media, and the study authors don’t mention women in any of them that we’ve seen. The results are reported as if they apply to everyone regardless of sex. Usually a reporter might pick up on such a detail and ask a question about it, but in this case the study authors hit the media before their study was posted online, so reporters didn’t have a chance to read it.
It’s an important and worrying omission for several reasons:
Women have been poorly served by medical science, which has often used male subjects for convenience, arriving at results which were just wrong for women. Caroline Criado Perez has recently published a book on this problem, Invisible Women, a section of which was published in Canvas magazine recently (March 23, 2019). In the UK Biobank study the authors had a large cohort of women – there were more women than men in the study – but as far as publicity was concerned they completely ignored the women’s distinctive results.
Women are more likely to be health-conscious than men (so far as we know, meat-eating hasn’t been associated with increased disease risk in the “health conscious” subgroups of the cohorts in any studies which apply this test). We know this generalisation is true from our work with What The Fat? and PreKure. This means that women are more likely to be aware of, and be influenced by, health messages in the media.
Women are more likely to be harmed by meat avoidance, because rates of iron and zinc deficiency are higher in women. B12 deficiency is also well worth avoiding. Fiona Greig, Beef and Lamb New Zealand’s well-informed head of nutrition, makes an especially good case in the Herald report on this study considering that she didn’t have access to the paper when she was asked to respond. Dr Felice Jacka who has studied the links between diet and depression for several years, including with a successful RCT, recommends 65-100g of red meat a day as part of the protocol for preventing anxiety and depression, which are strongly associated with meat avoidance. Misinforming women about the health effects of meat-eating has the potential to do real harm; let’s not forget that New Zealand is facing a mental health crisis, and that our government has set “wellness” as a target.
An additional reason that the null association in women should have been reported is, that it informs our confidence in the association being causal. Consistency and coherence are Bradford Hill criteria useful in assessing the links between association and causation. Completely different results for men and women are inconsistent (as are the results of other studies with no CRC associations for red meat, such as EPIC-Europe, or no cancer association for processed meat, such as the recent Seventh Day Adventist study). Nor does this give a coherent picture; this is not how “carcinogens” are expected to behave.
What about fibre?
In both men and women, grain fibre was associated with a 14% lower risk of colorectal cancer. Does this mean we all need to eat wholegrains? Not so fast – remember that the questionnaire collected data on many foods, including “white” carbs – white bread, white rice, pasta, pastry, and so on, as well as sugar. As the study was a UK study, total fibre intakes were pretty low by world standards. In the UK white bread is supplemented with folic acid (though this only became mandatory in 2018), and long-term exposure to high doses of folic acid (i.e not its temporary use in pregnancy, which is safe and beneficial) is also believed to be something of a risk factor for colorectal cancer (one reason folic acid fortification of bread, though usual, isn’t yet mandatory in NZ). Folate, the slow-release form of folic acid found in whole foods, is not thought to increase risk, and wholegrain bread doesn’t need to be fortified.
So were refined carbs, like white bread and sugar, associated with CRC in UK Biobank? We just don’t know; maybe this will be the subject of a future paper. In the EPIC-Italy cohort, from 2017, we find that “High intake of carbohydrate from high GI foods was significantly associated with increased risk of colon and diabetes-related cancers, but decreased risk of stomach cancer; whereas high intake of carbohydrates from low GI foods was associated with reduced colon cancer risk.” Which figures.
Because, what do we know with certainty about the causes of increases in CRC risk? Genetics plus ageing mean that cancer risks are never non-existent, but there are three factors the avoidance of which should keep them low –
High insulin. Fasting insulin is associated with CRC risk, and central obesity, type 2 diabetes, and the metabolic syndrome increase the risk of colorectal cancers. “Greater WC [waist circumference] and WHR [waist-to-hip-ratio] were significantly associated with increased risk of total colorectal cancer (WC: RR 1.42, 95% CI 1.30, 1.55; WHR: RR 1.39, 95% CI 1.25, 1.53), colon cancer (WC: RR 1.53, 95% CI 1.36, 1.72; WHR: 1.39, 95% CI 1.18, 1.63), and rectal cancer (WC: RR 1.20, 95% CI 1.03, 1.39; WHR: RR 1.22, 95% CI 1.05, 1.42).” 
Micronutrient deficiencies. Low selenium status, and low levels of PLP, the active form of B6, have been associated with increased CRC risk, and no doubt other micronutrient associations can be found. New Zealand is known for its low soil selenium status and high rates of bowel cancer. The risk is highest in the South Island, where selenium levels are lower because more imported food is eaten in the North.
Higher SePP concentrations were inversely associated with CRC risk (ptrend = 0.009; per 0.806 mg/L increase, IRR = 0.89, 95% CI: 0.82–0.98) with the association more apparent in women (ptrend = 0.004; IRR = 0.82, 95% CI: 0.72–0.94 per 0.806 mg/L increase) than men (ptrend = 0.485; IRR = 0.98, 95% CI: 0.86–1.12 per 0.806 mg/L increase). The findings indicate that Se status is suboptimal in many Europeans and suggest an inverse association between CRC risk and higher serum Se status, which is more evident in women.
Carcinogen exposure. This is the obvious one, one that is easy to overlook because it’s difficult to measure in a FFQ. But think about who works more in these kinds of industries – men or women? What are they likely to eat? Are these industries that will attract many vegans or vegetarians?
This work pointed out increased risks of colorectal cancer for labourers occupied in industries with a wide use of chemical compounds, such as leather (RR = 1.70, 95%CI: 1.24-2.34), basic metals (RR = 1.32, 95%CI: 1.07-1.65), plastic and rubber manufacturing (RR = 1.30, 95%CI: 0.98-1.71 and RR = 1.27, 95%CI: 0.92-1.76, respectively), besides workers in the sector of repair and installation of machinery exposed to asbestos (RR = 1.40, 95%CI: 1.07-1.84). 
And maybe it’s the oil too – in the recent China study RCT co-authored by Otago’s Jim Mann, a diet high in soybean oil, which is toxic to gram-positive bacteria, caused changes in the gut microbiome that have been associated with a higher CRC risk. It’s early days for this question, but we don’t recommend the extensive use of vegetable seed oils for a number of good reasons, hence “low carb healthy fat”.
The question of meat
We’re not concluding that meat, along with some other far less nutritionally valuable foods, can’t contribute to colorectal cancer, in men or women. Cooking methods might matter, as charred meat contains small amounts of chemicals called HPAs, which are carcinogens in high concentrations (interestingly HPAs are neutralised in the gut by acrolein, a carcinogenic toxin in its own right at high levels, which is formed by the burning of fat, by the beneficial probiotic Lactobacillus Reuteri, and by normal metabolic processes – clearly an example where the dose, and the context, makes the poison). High intakes or serum levels of iron are also possibly cancer promoting, but the differences between meat intakes in UK Biobank don’t seem large enough to be explained in this way. Nor does iron retention explain the difference between men and women, as the average age at the start of the study was 55 and the majority of women had passed through menopause. Blood donation, which significantly lowers iron levels, is associated with a reduced risk of some diseases – but not colorectal cancer.
It may also be relevant that some processed meats, especially those which go through “wash” processes, are very poor sources of micronutrients when compared with their unprocessed equivalents, with vitamins and minerals being lost during processing. Meat is a source of many of the micronutrients and amino acids involved in detoxification and antioxidant defense, including selenium. Thus if red meat does have an effect on cancer, this is likely to be bidirectional, which would be less true for some processed meats.
If anyone on a low carbohydrate diet is convinced by the reduced CRC risk associated with grain fibre, which is also seen in other studies for other diseases, and unconvinced by the argument that this just shows the same benefit of avoiding refined grains that we’re already enjoying, organic oat bran can be added to mince dishes such as patties and meatloaf, and makes an ideal binder.
Note that the richest animal food sources of saturated fat, the dairy products, were not associated with CRC in this paper (and usually have protective associations); higher HDL and the log[TG/HDL] ratio (AIP) were associated with lower CRC risk in EPIC-Europe in fully adjusted models, as was higher cholesterol before adjustment.
(Oh, also – fibre from fruit and vegetables not associated with cancer risk – what’s that about, 5+? It’s a fairly common finding in epidemiology, weak or no protective association for fruit and/or vegetables, but it never makes the news. When it contradicts the received version, we’re supposed to ignore science. So, eat your veges – after all, you have to eat something, and they’re going to be better for you than refined carbs!)
1] Kathryn E Bradbury, Neil Murphy, Timothy J Key, Diet and colorectal cancer in UK Biobank: a prospective study, International Journal of Epidemiology, , dyz064, https://doi.org/10.1093/ije/dyz064
2] Sieri S, Agnoli C, Pala V, et al. Dietary glycemic index, glycemic load, and cancer risk: results from the EPIC-Italy study. Sci Rep. 2017;7(1):9757. Published 2017 Aug 29. doi:10.1038/s41598-017-09498-2
3] Dong Y, Zhou J, Zhu Y, et al. Abdominal obesity and colorectal cancer risk: systematic review and meta-analysis of prospective studies. Biosci Rep. 2017;37(6):BSR20170945. Published 2017 Dec 12. doi:10.1042/BSR20170945
4] Hughes DJ, Fedirko V, Jenab M et al. Selenium status is associated with colorectal cancer risk in the European prospective investigation of cancer and nutrition cohort. International Journal of Cancer, Volume136, Issue5, 1 March 2015 Pages 1149-1161
First published: 09 July 2014 https://doi.org/10.1002/ijc.29071
5] Oddone E, Modonesi C, Gatta G. Occupational exposures and colorectal cancers: a quantitative overview of epidemiological evidence. World J Gastroenterol. 2014;20(35):12431–12444. doi:10.3748/wjg.v20.i35.12431
6] Engels C, Schwab C, Jianbo Zhang J, et al. Acrolein contributes strongly to antimicrobial and heterocyclic amine transformation activities of reuterin. Scientific Reports volume 6, Article number: 36246 (2016).
7] Zhang X, Ma J, Wu K, Chan AT, Fuchs CS, Giovannucci EL. Blood donation and colorectal cancer incidence and mortality in men. PLoS One. 2012;7(6):e39319. doi:10.1371/journal.pone.0039319
8] Sobiecki, J.G. Vegetarianism and colorectal cancer risk in a low-selenium environment: effect modification by selenium status? A possible factor contributing to the null results in British vegetarians. Eur J Nutr (2017) 56: 1819.
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Gut. 2011 Aug;60(8):1094-102. doi: 10.1136/gut.2010.225011. Epub 2011 Mar 7.
This is well worth the watch. Some NZ twists in here from our team and the battles going on (see the last post for more on the spoiler plays against low carb and diabetes reversal coming out of NZ that were mentioned by Aseem)
We were surprised to hear this Radio New Zealand interview with Jim Mann regarding a Chinese study he co-authored. In it he predicts various terrible things for people eating LCHF diets, which we think is out of line and not supported by the study.
In fact, the LCHF and Paleo community have been warning about exactly the type of diet that was used in the study – high in energy from soybean oil, rice, and wheat – for years, and Jim Mann’s crowd have attacked us for that, while the NZ Ministry of Health and Heart Foundation they advise has actively promoted such a diet. So it’s ironic that, as soon as we’re proved right, this is presented as evidence against our own, quite different advice – rather than being acknowledged as the humbling result it is for those supporting the current guidelines.
“Of particular interest was what happened to the bacterial flora of the gut, the microbiome underwent radical changes in these three different groups.
The low fat group had a bacterial profile which was compatible with low risk of a number of western diseases: heart disease and cancer.
The high fat group had a very different profile of bacteria in their gut, one more compatible with an increased risk of bowel cancer and also a much higher risk of inflammation leading to cardiovascular disease, heart disease and possibly diabetes,” Prof Mann says.
The results, he says, were “pretty scary.”
“It’s a strong message for what is happening in China, but I believe also a strong message for New Zealand and other similar countries where at least some people believe there are benefits to a high fat diet.”
All three groups had consistent and similar intake of vegetables, he says.
“A lot of people have argued you can have a high fat diet as long as you have a lot of veggies, I think that’s a serious misapprehension. If you are having a really high fat diet you’re not going to get a high fibre diet at the level of fibre that will be protective against these diseases.”
So what was the study?
“In a 6-month randomised controlled-feeding trial, 217 healthy young adults (aged 18–35 years; body mass index <28 kg/m2; 52% women) who completed the whole trial were included. All the foods were provided during the intervention period. The three isocaloric diets were: a lower-fat diet (fat 20% energy), a moderate-fat diet (fat 30% energy) and a higher-fat diet (fat 40% energy). The effects of the dietary interventions on the gut microbiota, faecal metabolomics and plasma inflammatory factors were investigated.”
The most important part of the paper is this statement:
Notably, the predicted lipopolysaccharide biosynthesis and arachidonic acid metabolism pathways were also increased in response to the higher-fat diet. Lipopolysaccharide is known to induce the release of arachidonic acid and its inflammation-involving metabolites, such as prostaglandins, thromboxane and leukotrienes. It should be noted that the intake of polyunsaturated fatty acids (PUFAs) was relatively high in the higher-fat diet group (24% of total energy) owing to exclusive use of soybean oil, which is rich in n-6 PUFA. A higher intake of n-6 PUFA has been reported to have proinflammatory effects.
In the interview, host Jesse Mulligan, who is a chef and knows his oils, does a great job of extracting this part of the story from Prof Mann. The n-6 (omega-6) PUFA in soy and other seed oils is linoleic acid; linoleic acid is the precursor of arachidonic acid (AA) and high levels drive AA synthesis. Lipopolysaccharide is also known as endotoxin and is a product of gram-negative bacteria that stimulates an immune response if it enters the bloodstream; a little endotoxin seems to be beneficial, but a lot can drive inflammatory diseases by activating the TLR4 receptor on immune cells.
Now, the traditional Chinese diet varies across regions so that it is hard to generalise, but the low fat Southern version looks like this – lots of green and coloured vegetables ( a very wide diversity, not just a large quantity), nose-to-tail meat (mostly pork and chicken), eggs, legumes, and white rice. Though low in fat, it can be relatively high in cholesterol due to the use of organ meats. Cooking can be by steaming, or stir-frying using small amounts of various oils. The dietary transition has seen more deep-frying in oils and the use of more oils in processed foods. Most of this is soybean oil (the majority of the soy grown in the former Amazon rainforest is now exported to China where it is used to make oil and soy protein, some of which is no doubt exported to NZ and the Pacific).
The equivalent of a 40% seed oil diet in NZ would be deep fried meals from KFC, plus Best Foods mayonnaise – popular foods in the more deprived areas of NZ.
Now, why would a high fat diet be bad for the microbiome? A moment’s thought will show that this doesn’t make sense as a generalisation. The microbiome is established in infancy, starting with birth when bacteria are transferred from the mother. The diet in infancy for mammals is, by definition, milk, a food always high in saturated fat and low in polyunsaturated fat. At day 16, human breast milk is 54% fat; of this fat 44.6% is saturated, 37.6% is monounsaturated, 14.6% is polyunsaturated omega-6 and 3.1% is omega-3. in hunter-gatherer populations without access to seed oils the omega-6 content is lower – e.g. 10% in the Tsimane of Bolivia vs 18% in the population of Cincinnati, USA.
Breast milk contains small amounts of soluble fibre, and lactose which lactobacillus can ferment but which is mostly absorbed and used for energy and growth.
However – lactobacillus also metabolise saturated fats. And some lactobacillus species make saturated fats that many other bacteria rely on between meals – these are the odd-chain fatty acids, C15 and C17, which you’ll find in dairy, beef, and lamb fat, but other dietary saturated fats can substitute for C15 and C17 when their production is disrupted by alcohol.
Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis* and reduces ethanol-induced liver injury in mice.
(*Eubiotics (Greek eu = good/healthy, bios = life) is the science of hygienic/healthy living. The term is used in the feed industry where it refers to a healthy balance of the microbiota in the gastrointestinal tract.)
And really, this should be obvious – if you buy yoghurt, the original probiotic food, you will find only two types to choose from – that made from milk (the animal food highest in saturated fat), and the vegan yoghurt made from coconut (the plant food highest in saturated fat).
Don’t blame the butter for what the soyabean did.
It has been known since 1945 that polyunsaturated fatty acids are toxic to lactobacillus and other gram-positive bacteria. In the China trial, the high soybean diet decreased levels of the gram-positive bacteria, Faecalibacterium, and increased levels of the gram-negative bacteria Bacteroides and Alistipes. A 2018 review  stated that:
Linoleic acid and the other two major unsaturated FAs in SBO, oleic acid (18:1), and alpha-linolenic acid (18:3), are known to be bacteriostatic and/or bactericidal to small intestinal bacteria as non-esterified (free) fatty acids in vitro at concentrations found in the small intestine (Kabara et al., 1972; Kankaanpää et al., 2001; Kodicek, 1945; Nieman, 1954). The primary modes of killing include permeabilization of cell membranes (Greenway and Dyke, 1979) and interference with FA metabolism (Zheng et al., 2005). Affected microbes are predominantly Gram-positive bacteria including the genus Lactobacillus (Nieman, 1954). Lactobacilli are particularly important as they are considered beneficial members of the human small intestine (Walsh et al., 2008; Walter et al., 2007; Walter et al., 2011). They have been shown to be growth inhibited by the specific FAs present in SBO (Boyaval et al., 1995; De Weirdt et al., 2013; Jenkins and Courtney, 2003; Jiang et al., 1998; Kabara et al., 1972; Kankaanpää et al., 2001; Kodicek, 1945; Raychowdhury et al., 1985). It is interesting to note that the human-associated L. reuteri underwent a population bottleneck that coincides with the increase in SBO consumption in the U.S. and is far less prevalent than it was in the past (Walter et al., 2011). In the 1960’s and 1970’s prior to the emergence of SBO as a major dietary fat source, L. reuteri was recovered from the intestinal tract of 50% of subjects surveyed and was considered a dominant Lactobacillus species of the human gut (Reuter, 2001). Today, however, it is found in less than 10% of humans in the USA and Europe (Molin et al., 1993; Qin et al., 2010; Walter et al., 2011), yet it is present at a reported 100% prevalence in rural Papua New Guineans (Martínez et al., 2015).
Yet the paper Jim Mann co-authored cites none of this research. There is only one reference in it (46) to the possibility that a high omega-6 intake can be inflammatory, and this review does not mention the effect on the microbiome – despite being written by microbiologists.
This sort of thing is all-too common – a lack of curiosity in nutrition research. To plan an experiment like the Chinese soybean oil trial takes years. If you’re planning to feed an unusual amount of linoleic acid – 24% of energy – to people and measure its effects on the microbiome, why are you not curious enough to search for the evidence about the effect of linoleic acid on the microbiome? If you think more fat is bad fat, whatever its composition, you might miss this step. It’s possible that reference 46 and the comment about linoleic acid was added by a reviewer and was not even part of the paper as originally submitted. Or, it might have been included by Jim Mann, who is not a complete fool and who has long been exposed to Paleo arguments about omega-6, but went over the heads of his coauthors, the microbiologists.
So the microbiome results are no surprise to us (though predicting disease from the microbiome at our present stage of knowledge would be about as reliable as predicting it from tea leaves or tarot cards, gram-positive lactobacillus and bifidus probiotics have been well-tested and are for example associated with a reduction in rehospitalization for mania in bipolar disorder, HR 0.26, 95% confidence interval [CI] 0.10, .69; P = .007).
But what is surprising, and should have surprised Jim Mann, is that LDL cholesterol did not go down on the high-PUFA diet. After all, the effect of PUFA on cholesterol has been the excuse for promoting these oils. There is increasing doubt about whether the effects of fat (amount or type) on LDL cholesterol counts has any important influence on CVD risk in the first place, but the news that soybean oil has no effect on LDL in a real world experiment means that there is no longer any rationale for recommending it.
So come on. This isn’t good interpretation of the results. The results of this high-soybean oil study say nothing about the effects of high fat diets when those fats are traditional fats that are not toxic to beneficial bacteria. The results of this study, where more energy came from carbs (mainly wheat and rice) than from fat, can say nothing about LCHF diets where wheat and rice are avoided or limited. Jim Mann’s comments about “the level of fibre that will be protective against these diseases” are based on epidemiology where very high levels of fibre are associated, not with IBD as in the real world, but with protection against all sorts of diseases. But we have news for him – very high levels of linoleic acid were also protective in epidemiology. Just not in the real world. The majority of associational results discovered in epidemiology are not borne out by later experiments, because associational epidemiology is inherently inaccurate, and can reflect the bias of epidemiologists, who are today also influencers of the populations they study.
Postscript: The results of this study can help us to understand one of the more interesting nutritional epidemiology papers. The Malmo Diet and Cancer Study (MDCS) is a large cohort study that uses a 7-day food diary to collect data and also has stricter validation criteria than FFQ research, putting it into the highest category of evidence for such studies. In the MDCS, of 8,139 male and 12,535 female participants (aged 44–73 y), there were 1,089 male and 687 female iCVD cases (Ischemic cardiovascular disease, including strokes and heart attacks) during a mean 13.5 year follow-up. That’s about 1 in 8 men and 1 in 20 women. For iCVD, after full adjustment, fiber intake was negatively and significantly associated with iCVD in women (24 percent lower risk in the highest intake quintile compared to the lowest, 95 percent confidence interval −3 to −41 percent, p for trend = 0.022), but no other significant associations were noted, except a borderline (p=0.050) protective association of fibre with stroke for men. But here’s where it gets interesting – in the post-hoc analysis, adjusting for the other nutrients revealed that the combination of high fibre and high saturated fat was protective; that is, for men lowest quintiles of SFA and fibre combined had statistically significant HRs for iCVD of 1.82, which is pretty high, whereas high fibre/low SFA and high SFA/low fibre had the reference 1. For women, the lowest risk of iCVD, 0.36, was in the highest fibre, second highest SFA quintile, with the highest SFA highest-fibre quintiles being similar but non-significant.
This result makes sense if both fibre and saturated fats are prebiotic foods, and if the combination supports eubiosis better than the combination of fibre and unsaturated fats.
 Wan Y, Wang F, Yuan J, et al Effects of dietary fat on gut microbiota and faecal metabolites, and their relationship with cardiometabolic risk factors: a 6-month randomised controlled-feeding trial. Gut Published Online First: 19 February 2019. doi: 10.1136/gutjnl-2018-317609
 Marshall JC. Lipopolysaccharide: an endotoxin or an exogenous hormone? Clin Infect Dis. 2005 Nov 15;41 Suppl 7:S470-80.
 Jensen RG. Lipids in human milk. Lipids 1999 Dec;34(12):1243–71. http://pmid.us/10652985
 Martin MA, Lassek WD, Gaulin SJ, et al. Fatty acid composition in the mature milk of Bolivian forager-horticulturalists: controlled comparisons with a US sample. Matern Child Nutr. 2012;8(3):404-18.
 Chen P, Torralba M, Tan J, et al. Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis and reduces ethanol-induced liver injury in mice. Gastroenterology. 2014;148(1):203-214.e16.
 Kodicek E. The effect of unsaturated fatty acids on Lactobacillus helveticus and other Gram-positive micro-organisms. Biochem J. 1945;39(1):78-85.
 Di Rienzi SC, Jacobson J, Kennedy EA, et al. Resilience of small intestinal beneficial bacteria to the toxicity of soybean oil fatty acids. Elife. 2018;7:e32581. Published 2018 Mar 27. doi:10.7554/eLife.32581
 Dickerson F, Adamos M, Katsafanas E. Adjunctive probiotic microorganisms to prevent rehospitalization in patients with acute mania: A randomized controlled trial.
Bipolar Disord. 2018 Nov;20(7):614-621. doi: 10.1111/bdi.12652. Epub 2018 Apr 25.
 Ioannidis JPA. The Challenge of Reforming Nutritional Epidemiologic Research. JAMA. 2018;320(10):969–970. doi:10.1001/jama.2018.11025
 Wallström P, Sonestedt E, Hlebowicz J, et al. Dietary fiber and saturated fat intake associations with cardiovascular disease differ by sex in the Malmö Diet and Cancer Cohort: a prospective study. PLoS One. 2012;7(2):e31637.
SCIENCE IN A MINUTE: @Caryn Zinn Nutrition reviews the latest Lifestyle Medicine research released two weeks ago in the British Medical Journal (BMJ) on weight-loss maintenance.
Which diet works best for maintaining weight loss? Find out…
What’s more important to you – your left arm or your right foot? What would you rather keep if you had to lose one or the other?
Well, here’s my opinion in the video below and longer blog here
Actually it’s all about how we need to talk about fitness more. Fitness is medicine. Enjoy…and get fit!
You will see yourself linked to Prekure’s www site. Prekure – “prevention is cure” is a social enterprise I’m part of with 8 other health professionals from oncology to public health to general practice to pharmacy.
We are hoping to make a dent in medicine – to move from drugs as frontline treatment, to lifestyle as first line medicine. The social arm offers free lifestyle medicine programs which really work, available for everyone. We are also doing medical education training for health professionals – in lifestyle medicine, of course. We want to bring today’s evidence to the front line of healthcare – its compelling.
We’ve just got going. Stay tuned and please join our community to change medicine to “prevention as cure”. More to come.
Prekure’s social links below
Here’s a little piece I wrote for the Education sector in the Education Gazette, around the big issues for our kids..
Opinion piece: By Grant Schofield, Professor of Public Health and Director of the Human Potential Centre at AUT Millennium, and the Ministry of Education’s Chief Education Health and Nutrition Advisor.
What should a rich, developed country like New Zealand be aspiring towards? I think having a good life for all would be a great aspiration.
But what’s a good life?
A good life starts with having the health to physically and mentally do whatever else you want to. Without that base, you have very little to go on with.
New Zealand’s report card looks pretty poor as far as ‘good health’ is concerned. Yes, we live longer than we ever have, but our healthy life expectancy hasn’t kept up. There’s now a big gap between actual life expectancy and ‘healthy’ life expectancy. Men average 79 years of life, but just 65 of healthy life. Women average 83 years, with 66 healthy. Māori men average 72 years with just 54 years healthy.
And…we spend $18.1 billion on health. But the reality is that almost all of those billions go on sorting out sickness. That sickness system is helping us have longer lives but not necessarily better lives.
Why I am writing this in the Gazette? Shouldn’t we be focused on young people, not old people, as educators?
Well, if we want to change the behaviours that really determine our health, we are going to have to look outside the health system. And we are going to have to start with young people.
The five big things that affect our healthy life are all set up when we are young. It’s about not smoking, less alcohol, better nutrition, better sleep, and how much we move (more activity). We’ve made great progress on smoking and to an extent alcohol harm, but nutrition, sleep, and physical activity are all arguably getting worse.
A recent PISA report from the OECD tells us that exercise and activity are important for the wellbeing of our youth.
Here’s the top four challenges I think we all face in boosting our young people’s health and wellbeing, and ultimately that of society:
Challenge 1: Mobile devices
They are pretty much the most useful device invented. You carry instant access to all the knowledge of humanity in your hand. Awesome. And they are awesome tools. The mobile is a great servant, yet a hideous master.
High device use disrupts sleep quantity and quality, reduces activity, and has the potential to disrupt genuine experiences with friends, and promote bullying. Understanding how to effectively use, but contain mobile devices, in our young people is the critical challenge of our time. As parents and educators, let’s help ourselves too. Let’s model what we want to see in our youth.
Challenge 2: Getting outside
Getting outdoors and moving is effective in improving mood, reducing depression, improving academic performance, and improving sleep. This can easily be a priority in education. Scientifically it makes sense. My challenge to you is how to build this into the rest of your curriculum delivery. The Hauora aspects of the HPE curriculum lend achievements in this curriculum and learning area to also achieving across multiple other areas of literacy, numeracy and inquiry.
Can you take some of your teaching outside and have physical activity involved?
Challenge 3: Free-range kids
Risk and adventure on your own terms is part of growing healthy kids. We now know that frontal lobe development (read self-control and risk management) develops when you engage in unstable outdoor activity. That means play with consequences. Playstations do not help this development. There are no consequences when you crash your car on Grand Theft Auto. There are consequences for poor tree climbing skill.
Schools can allow tree climbing, adventurous and vigorous play, and even some full contact games. I’m not talking about negligence. I’m talking about helping children learn about risk before they are driving a car and exposed to drugs and alcohol as teenagers. We have a choice in society when we learn this. The earlier the better in my opinion.
Challenge 4: Food
It’s pretty obvious that the modern, industrial food supply bears little resemblance to what humans have eaten for most of the time we’ve been on the planet. Highly processed and packaged food is bad for the youth brain, body, learning and their mental health. There is so much infighting and confusion in nutrition science, but one thing we all agree on is that whole unprocessed food is the way to go.
That’s why I’d like to introduce you to the ‘HI’ (Human Interference) factor. The guide to healthy eating need not get into the ins and outs of fats, carbs, sugars and so on. All we need to ask ourselves is, “Was this plant/animal recently alive in nature running around or growing somewhere?” Yes = eat it. No – it doesn’t resemble anything recently alive = don’t eat it. If we can start a movement around this approach, we will be most of the way to eating healthy again. Big Food companies, who market highly processed, sugary foods won’t like this one bit. In my opinion, Big Food shouldn’t be welcome in our schools. They are behaving exactly like Big Tobacco did – creating confusion, buying science, giving misinformation, and associating themselves with sport and young athletes.
That’s it. Challenges, not answers.
Once again we have headlines about how we need to cut back on meat consumption for the sake of our health, and the planet’s, fueled by a recent review. We’ve addressed the climate effects of ruminant agriculture before, this (most particularly with regard to intensive dairying and least of all with regard to sheep) is a conversation we need to keep having in NZ, but we would prefer experts to stop conflating this agenda with health advice.
As we’ll show, no-one has good data about how much meat New Zealanders currently eat, but past figures show that large numbers of Kiwis were deficient in the very nutrients that meat supplies in goodly amounts, making overconsumption unlikely. We’ll also present evidence that meat avoidance may have serious effects, which our health authorities may be overlooking.
It is not our position that vegetarian and vegan diets are intrinsically harmful; educated people with sufficient income, or people with sound cultural support in the case of traditional vegetarian diets, are those most likely to eat nutritionally adequate diets without meat, or with little meat. But meat and other animal foods are so nutrient dense as to be dietary fail-safes for the majority of people who do not have time, inclination, money, or education to guarantee good nutrition otherwise, as we will see. Random advice to cut these foods from the diet, delivered without nuance as primetime TV News, can only harm the most vulnerable members of society.
How much meat is in our “high meat” diet?
New Zealand authorities have not calculated the amount of meat in our diets since the 2008/2009 Health and Nutrition Survey. (another survey was done since, but the only diet questions in it were about one about sugary soft drink consumption and one about getting 5+ servings of fruit and vegetables a day).
According to the 2008/2009 nutrition survey, the protein intakes estimates of New Zealanders were 16.4% and 16.5% of energy for males and females respectively, at the lower end of dietary recommendations of 15-25%.
Bread and other grain-based foods supplied nearly a third of our protein intake, only a fifth of which came from red meat, processed meat, and pork. (We calculate this as an average of only 16.5 grams of meat protein per day in a 2,000 kcal diet).
Similarly, meat contributed significantly less iron to the diet (about 13%) than bread, pasta, and breakfast cereals (29%). These figures do not indicate a population overeating meat; if anything, they seem to indicate a population overly reliant on refined wheat in all its forms (only the processed forms of grains, which are supplemented, are a good source of iron).
When these results were published in 2011, Professor Elaine Rush, Professor of Nutrition, Faculty of Health and Environmental Science, Auckland University of Technology made the following comments on the Science Media Centre blog:
The biggest whammy is for people living in more deprived areas. They are more likely to be overweight or obese, not meeting recommended micronutrient intakes such as iron, vitamin A and calcium. Bread continues to be the major contributor of energy, protein, and carbohydrate to the New Zealand diet, In comparison to white bread, light or heavy whole grain bread was chosen by 60% of the population, but almost 50% of young adults compared to 25% of older people reported eating white bread. The most socioeconomically deprived 20% were twice as likely to consume white bread compared to the most well off 20% (20% vs 40%).
The evidence is clear, in 2008 New Zealanders were not well nourished, many did not have enough money to buy nutritionally adequate and safe foods and were not healthy. Since then the economic recession and the ever-increasing cost of food mean that we are unlikely to be improving. More importantly our present children and those still to be conceived are not likely to have an optimal start to life continuing the cycle. A whole of New Zealand response is required because it is not a personal choice or responsibility- particularly for children. We produce enough good food to feed everyone well – why the gap between the farm and the mouth?
Why indeed? Our red meat exports are higher than ever, yet this seems to be diverted away from our population. Zinc seems to be very much an indicator of animal food (red meat, shellfish, and cheese) consumption in the MOH report, as no good plant sources of zinc are listed.
Nearly a quarter (24.7 percent) of New Zealanders aged 15 years and over were not getting enough of the trace element zinc in their diet, with 39.1 percent of men and 11.2 percent of women missing out. The median usual daily intake of zinc was 12.9mg for men and 9mg for women, and even lower for older people. These intakes were down on those seen in the 1997 survey.
As the RDI of zinc is 14mg per day for men and 8mg/day for women, this means that most men and almost half of women in NZ were below the RDI for zinc in 2008/2009. Hardly a population eating too much meat back then, but we don’t know if this is even worse today. And there’s the problem – experts racing off making blanket recommendations when there is insufficient data about the current position.
Adverse effects of meat avoidance – mental health.
We have serious concerns about the effect of meat avoidance at a population level as a public health-endorsed recommendation, whether the reason for it is ethical, socio-political, environmental, or flat-out poverty. Such advice needs to meet robust criteria for cause and effect, the effect needs to be strong and with little chance harm occurring with populations taking such recommendations.
The study by Hibbeln et al that found increased rates of depression in vegetarian men cites six other studies with similar findings, including two in adolescents. Only one cited study, in US Seventh Day Adventists – a relatively privileged group which plays an important role in the promotion of meat avoidance – had different results.
Another study by Hibbeln et al found that vegetarianism in pregnancy was associated with substance abuse (alcohol and cannabis) in offspring, and screening for the effect of a vitamin B12 absorption allele increased confidence that the relationship was causal (there was no association by diet in those who had genetically poor B12 absorption whatever their diet).
A survey of patients with anorexia nervosa found that vegetarians and vegans were over-represented and were more likely to have a persistent condition.
Compared to controls, individuals with an eating disorder history were significantly more likely to ever have been vegetarian (52% vs. 12%), to be currently vegetarian (24% vs. 6%), and to be primarily motivated by weight-related reasons (42% vs. 0%). The three recovery status groups (fully recovered, partially recovered, active eating disorder) did not differ significantly in percentiles endorsing a history of vegetarianism or weight-related reasons as primary, but they differed significantly in current vegetarianism (33% of active cases, 13% of partially recovered, 5% of fully recovered). Most perceived that their vegetarianism was related to their eating disorder (68%) and emerged after its onset.
The associations between meat avoidance and mood disorders in these studies are strong – they certainly dwarf any associations drawn between meat and any other diseases. We acknowledge this alone doesn’t demonstrate cause and effect. But it does suggest that there is a possibility of harm, and we must be cautious with population-wide advice.
New Zealand needs data on these correlations from within its own population before our public health experts start recommending meat avoidance to a population which has so many vulnerable members, in a country which is facing a mental health crisis.
Meat and cancer, Part 2 (Part 2).
The review goes lightly into the meat and colon cancer association, without a very clear discussion of the stats or the hopelessness of the “processed meat” definition. We’ve discussed this data before, but we’d like to share a much stronger and more convincing association – in 2006 people being treated for colon cancer, the insulin load and insulin index of the diet (a measure of the amount of insulin required to metabolise the food) was strongly correlated with cancer mortality.
The adjusted HRs for CRC-specific mortality comparing the highest to the lowest quintiles were 1.82 (95% CI: 1.20-2.75, Ptrend=0.006) for dietary insulin load and 1.66 (95% CI: 1.10-2.50, Ptrend=0.004) for dietary insulin index. We also observed an increased risk for overall mortality, with adjusted HRs of 1.33 (95% CI: 1.03-1.72, Ptrend=0.03) for dietary insulin load and 1.32 (95% CI: 1.02-1.71, Ptrend=0.02) for dietary insulin index, comparing extreme quintiles. The increase in CRC-specific mortality associated with higher dietary insulin scores was more apparent among patients with body mass index (BMI)⩾25 kg m-2 than BMI<25 kg m-2 (Pinteraction=0.01).
Now, while it’s true that protein requires insulin to be metabolised and that beef has a relatively high insulin load, it is also true that people eating low-carb diets get insulin levels very low whether they eat meat or not; such diets certainly reverse hyperinsulinaemia. Refined carbs are simply going to drive up the insulin effect of other foods like beef; you need protein and vitamins and minerals, and you don’t need sugar and artificial colourings.
It’s refined carbohydrate, sugar and starch, not protein or fat, which is most likley wasting the health of New Zealanders. We can demonstrate this by the improvements in health we see every day when people limit sugar and starch in their diets; not just biomarkers, but improvements in mood, pain, and exercise capacity. The health benefits of carbohydrate restriction are becoming more generally known and accepted with time.
The realisation that sugar and starch are fundamental to the nutrition-related harm that occurs in populations of developed countries is becoming mainstream now. The recent BMJ special issue “Food for Thought” is swimming in the science and policy of such a realisation.
There may even be environmental benefits; for one thing, you can now eat the fat from an animal instead of wasting it and replacing it with another food, for another thing, weight loss is a common side-effect of LCHF, even when used as a migraine cure.
And excess weight means people need to eat more. In 2012, biomass due to obesity was 3.5 million tonnes, the equivalent of 56 million people of average body mass (1.2% of human biomass globally). If the obesity epidemic could be entirely reversed, the food savings would be roughly equivalent to the annual food consumption of Australia and Canada combined (minus that of little New Zealand). This is perhaps a drop in the bucket globally, but it is still a lot of people.
Of course, we can treat and farm animals better and be more sustainable. That’s what the apex omnivore – us humans – must do if we want to leave even a half decent planet for the next generations.
 Godfray HCJ, Aveyard P, Garnett T et al. Meat consumption, health, and the environment. Science. 2018 Jul 20;361(6399). pii: eaam5324. doi: 10.1126/science.aam5324.
 Hibbeln JR, Northstone K, Evans J, Golding J. Vegetarian diets and depressive symptoms among men. J Affect Disord. 2018 Jan 1;225:13-17. doi: 10.1016/j.jad.2017.07.051. Epub 2017 Jul 28.
 Hibbeln JR, SanGiovanni JP, Golding J, et al. Meat Consumption During Pregnancy and Substance Misuse Among Adolescent Offspring: Stratification of TCN2 Genetic Variants. Alcoholism: Clinical & Experimental Research. Published online October 4 2017
 Bardone-Cone AM, Fitzsimmons-Craft EE, Harney MB, et al. The Inter-relationships between Vegetarianism and Eating Disorders among Females. Journal of the Academy of Nutrition and Dietetics. 2012;112(8):1247-1252. doi:10.1016/j.jand.2012.05.007.
 Yuan C, Bao Y, Sato K et al. Influence of dietary insulin scores on survival in colorectal cancer patients. Br J Cancer. 2017 Sep 26;117(7):1079-1087. doi: 10.1038/bjc.2017.272. Epub 2017 Aug 17.