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.
Grant’s family and friends enjoy a day at Frog Rock in Hikuai, Coromandel.
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.
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, 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.
Here’s your chance everyone…The Australian and NZ governments are calling for public consultation on food labelling, especially around sugar.
The letter I got is pasted below. Make your submissions at this link
So, they are asking us what we think. Let’s not just complain afterwards…Have a go if you care about what we eat.
Dear Stakeholder The Food Regulation Standing Committee (FRSC) is inviting submissions from stakeholders on the labelling of sugars on packaged foods and drinks. A Consultation Regulation Impact Statement (Consultation Paper) has been prepared to seek information on this topic from stakeholders, including industry, public health and consumer organisations and other interested parties. The Consultation Paper is available on the Food Regulation website. As this is a public consultation, we ask that you forward this invitation to any other relevant parties that would be interested in providing a submission. Information provided in response to the consultation will be drawn upon to prepare a Decision Regulation Impact Statement which will identify a preferred policy option to recommend to the Australia and New Zealand Ministerial Forum on Food Regulation (the Forum) in relation to the labelling of sugars on packaged foods and drinks. The Forum is comprised of Ministers responsible for food regulation from the Australian Federal Government, New Zealand, and Australian States and Territories governments. Submissions need to be lodged through the online Portaland should be supported by evidence. Peak organisations are expected to consult their members on the questions in the Consultation Paper and provide a single response on behalf of their members. Duplicate submissions are not necessary. Submissions that are not evidence-based, or do not directly answer the questions in the paper may not be drawn upon in preparing the Decision Regulation Impact Statement for the Forum. Submissions close at 11.59pm on 19 September 2018 Australian Eastern Time. If you have any questions about this consultation process, please contact the Food Regulation Secretariat at the email address below. Thank you in advance for taking the time to make a submission. Kind regards Food Regulation Secretariat Website: www.foodregulation.gov.au | Email: FoodRegulationSecretariat@health.gov.au Phone: +61 2 6289 5128 | Postal Address: MDP 707, GPO Box 9848, Canberra ACT 2601
This is a good little watch. Last month I sat down with Todd Scott CEO of the National Business Review, and Chris Keall also at NBR. Chris had let his weight get away on him and needed to front up to this. Todd was in pretty good shape, but is always aiming to be a high performer. He was looking at a reset to be in his best possible shape.
So they took on a fasting challenge following our “super fasting” protocol in What the Fast?
Here’s the full article and video here, it’s a great little video of the outcomes 4 weeks later …some great men’s weight loss results for both Todd and Chris, as well as some interesting mental health (including medication reduction) outcomes for Todd.
Its the same stuff – saturated fat is bad for you. Avoid it, and replace it with polyunsaturated and monounsaturated fats
But hang on minute, is this still the best advice you have? And will it really prevent people getting cardiovascular disease?
The advice to limit saturated fat misses more important effects?
We think there are a few holes in the argument. Or at least we aren’t getting the full story.
“Substituting dietary saturated fat with mono and polyunsaturated fats is the most effective dietary approach to reducing low-density lipoprotein cholesterol (LDL-C) while maintaining or increasing high-density lipoprotein cholesterol (HDL-C).”
But we think this misses the mark – polyunsaturated and mono-unsaturated fats lower LDL because of their effect on the LDL-receptor and on ApoB catabolism. But they only raise HDL when substituted for carbohydrate, because they are fats, and fats in general stimulate the release of ApoA1, the seed of HDL, from gut and liver cells.
A high intake of linoleic acid lowered LDL and raised HDL when it was added to the baseline fat intake (e.g. replaced carbohydrate in the diet), but lowered both LDL and HDL when it replaced saturated fat.
This might seem to be picking on the details, but we think it is important. As it stands above replacing saturated fats isn’t the most effective way of changing the fats in your diet to improve your chances of avoiding clogged arteries.
We think better advice might to be to replace the carbs your eat with fats from minimally processed foods.
The classic feeding study meta-analysis of Mensink et al. makes clear the benefits of replacing carbohydrate with various fats. This is worth quoting at length.
The cis MUFAs had a modest but significant LDL cholesterol–lowering effect relative to carbohydrates. All 3 classes of fatty acids increased HDL cholesterol relative to carbohydrates. Unsaturated fatty acids increased HDL cholesterol less than did SFAs. As a result, the replacement of 1% of energy in the form of SFAs with an equal percentage in the form of cis MUFAs is predicted to lower HDL-cholesterol concentrations by 0.002 mmol/L. A similar decrease is expected when 1% of energy in the form of MUFAs is replaced with an equal percentage in the form of PUFAs. These effects, however, are small compared with those of replacement of carbohydrates with any of the 3 classes of fatty acids. Replacement of carbohydrates with any class of fatty acids decreased fasting serum TG concentrations (Table 1). The effect was slightly but not significantly larger for PUFAs than for other fatty acids. This contrasts with the powerful TG-lowering effect of n−3 PUFAs from fish, which is evidently not shared by linoleic acid, the major n−6 PUFA. Replacement of carbohydrates with SFAs did not change apo B concentrations. The cis unsaturated fatty acids, however, decreased apo B, and this effect was slightly stronger for PUFAs. SFAs and MUFAs increased apo A-I concentrations relative to carbohydrates. PUFAs did not significantly change apo A-I concentrations.
In other words, all benefits expected in terms of increasing unsaturated fats are seen when fat replaces carbohydrate, and this has the additional benefit of decreasing triglycerides – it’s better for the TG/HDL ratio. We explained how this effect plays out in terms of ApoB and ApoA1, even if saturated fat increases, in an earlier blog.
The substitution meta-analysis of Farvid et al makes it clear that a similar effect – an association with risk here, not just risk markers – is even seen in prospective cohort studies, confounded though those are.
“9 cohort studies evaluated substitution of LA for carbohydrate showed that substituting 5% energy intake from LA for carbohydrates lowered risk with about 10%. A slightly lower risk benefit was seen for substitution of LA for SFA.”
So if it’s better, or at least not worse, to replace carbs with unsaturated fats and leave saturated fats as they were, why isn’t this offered as advice?
The most at risk benefit the least from current advice
The problem with the existing advice is is, that even the expected effects of replacing SFA with unsaturated fats are unlikely to be seen if you are overweight or insulin resistant. The studies being relied on for guidelines are based, overall, on healthy volunteers – unfortunately for people depending on these results, insulin sensitive people are at very low risk of CVD, and LDL has little correlation with their risk, but the opposite is true for the insulin-resistant.
Design: A randomized, double-blind, 3-period crossover controlled feeding design was used to examine the effects on plasma lipids of 3 diets that differed in total fat: the AAD [designed to contain 38% fat and 14% saturated fatty acids (SFAs)], the Step I diet (30% fat with 9% SFAs), and the Step II diet (25% fat with 6% SFAs). The diets were fed for 6 wk each to 86 free-living, healthy men aged 22–64 y at levels designed to maintain weight. Results: Compared with the AAD, the Step I and Step II diets lowered LDL cholesterol by 6.8% and 11.7%, lowered HDL cholesterol by 7.5% and 11.2%, and raised triacylglycerols by 14.3% and 16.2%, respectively. The Step II diet response showed significant positive correlations between changes in both LDL cholesterol and the ratio of total to HDL cholesterol and baseline percentage body fat, body mass index, and insulin. These associations were largely due to smaller reductions in LDL cholesterol with increasing percentage body fat, body mass index, or insulin concentrations. Subdivision of the study population showed that the participants in the upper one-half of fasting insulin concentrations averaged only 57% of the reduction in LDL cholesterol with the Step II diet of the participants in the lower half.
Whereas the drops in HDL and rise in TG (from the stepwise reductions in fat and replacement with carbs) probably cancelled out any benefit from lower LDL in responders here, the most IR subjects weren’t even getting the benefit of lower LDL! That’s where a low carb approach to lipid management would have come in handy – if insulin and body fat % became lower, these subjects would experience a greater response to any PUFAs and MUFAs in their diet.
What is LDL anyway?
The LDL-cholesterol (LDL-C) in a standard lipid panel is just a calculated proxy for ApoB. On a low carb diet, with low TGs, you’ll start to get discordance between LDL-C and ApoB. That is, sometimes the LDL-C count can go up even when there’s a reduction in ApoB; this is because the ApoB particles become larger and less atherogenic. We see this in the Virta Health type 2 diabetes study – there’s a 9% rise in LDL cholesterol but ApoB has decreased non-significantly, LDL-P (the actual number of LDL particles) has decreased, small LDL-P (the actual number of the most atherogenic type of LDL particle) has decreased massively, and of course everything else has improved.
Curiously, triglycerides are only mentioned in the new guidelines as a risk factor for pancreatitis, which is one pathway to diabetes, and not as a CVD risk factor (and the cut off here is 11 mmol/L. Wow). We’re not sure why this is. Has the new shift to non-fasting tests made it impossible to use the old risk calculations, which clearly defined risk in terms of LDL, TG, and HDL? Is there an assumption that because everyone in NZ should be eating a high carb diet, there is no point giving advice to lower TGs? It’s a mystery. TGs (with more reasonable cut-offs) are still a risk factor for people with LDL controlled by statins.
Triglycerides are important
Here’s a rare, good quality study (n= 3590) from the Framingham Offspring Cohort that actually looked at risk based on all 3 lipid measures, in a population not taking any lipid-lowering drugs. The high/low cut of for HDL was 40 mg/dL for men and 50 mg/dL for women, which some labs will tell you is still too low (we can do better !). The lowest TG cut-off of 100 mg/dL is also a bit high (again, we can do better !) – the 2 cut-offs combined give a TG/HDL ratio of 2.5 for men and 2 for women, whereas the insulin-sensitive groupings in other studies tend to have a mean TG/HDL ratio of ~1.1 (consistent with LDL particle size in people with type 2 diabetes improving below a TG/HDL ratio of 1.5).
Even so, you can see that if HDL is high and TG low, risk is low, and any difference in the LDL level has little effect. Note that this population wasn’t screened for familial hypercholesterolaemia genes, which would have impacted risk across all higher LDL categories.
Statins – good for some?
When statins (okay we will wade into this just a little) are prescribed in secondary prevention (i.e. after a heart attack), they are very effective in preventing a second event in the most insulin-resistant people, calculated by the TG/HDL ratio. The NNT (number needed to treat) over 6 years in the IR group in the 4S study was 6, which is amazingly good – but statins didn’t really make much difference to the most insulin-sensitive, who are at an almost equally low risk if taking a placebo – their NNT in 4S was 36.
Remember, these insulin sensitive cases, who don’t seem to benefit much from LDL lowering, are also the ones likely to see the biggest LDL drop if they replace saturated fats with unsaturated fats (it’s the opposite with statins, so the insulin-sensitive people below were actually on a higher statin dose to get the same LDL reduction – so much for extrapolating between diet and drug effects).
Age increases risk?
It’s also worth questioning the use of age as a continuous variable in risk calculations. Of course your risk of dying from any disease goes up as you age, but trials of statins in elderly populations for primary prevention are few, and include 1) the ALLHAT open-label trial where statin use was not beneficial in a post-hoc analysis of the elderly patients (n=2867): this was a rare trial not funded by industry and came closest to a real-world model of prescribing.
The hazard ratios for all-cause mortality in the pravastatin group vs the UC group were 1.18 (95% CI, 0.97-1.42; P = .09) for all adults 65 years and older, 1.08 (95% CI, 0.85-1.37; P = .55) for adults aged 65 to 74 years, and 1.34 (95% CI, 0.98-1.84; P = .07) for adults 75 years and older. Coronary heart disease event rates were not significantly different among the groups.
2) The PROSPER RCT (n=5804) in which CHD was reduced, but all-cause mortality was not affected (0·97 (0·83–1·14)) due to increases in other causes of death.
3) The JUPITER and HOPE3 trials, in which a recent post-hoc sub-group meta-analysis has revealed benefit for the elderly patients. (JUPITER was a statin trial targeted at patients with low LDL but high CRP, i.e. inflammation, and had most clear evidence of benefit in cases with low HDL at baseline, which again is evidence of statins being far more effective in the insulin-resistant). The older people were, the more likely they were to stop taking statins, but we can’t say how much of this is due to increasing side effects with age, because side effects were poorly recorded in these early statin trials.
Risk management in the elderly may also be complicated by the fact that total cholesterol and LDL are often protective risk markers in older populations. For example, in the Danish registry of people without pre-existing heart disease or diabetes higher LDL is associated with lower mortality, compared with LDL under 2.5 mmol/L, in those over 50. That this included those with very high LDL – above 4 mmol/L – rules out reverse causality. Though statin use (by about 1 person in 4) was also associated with lower mortality in this population, there was no interaction between statin and cholesterol (i.e. statins didn’t explain the LDL difference either way). HDL between 1-2 mmol/L was protective compared with HDL <1 mmol/L (39 mg/dL); HDL ≥ 2 mmol/L was protective in women but not men (very high HDL levels can reflect heavy drinking), and higher TG was associated with increased mortality. In other words, the TG/HDL ratio – which correlates with fasting insulin, the 2-hour insulin response to glucose, and measures of insulin resistance – still predicted the risk of dying even in a population where LDL was pointing the other way.
Better diet prescription?
If we’re going to prevent diabetes and cardiovascular disease, it’s obvious we need to identify insulin resistance and prescribe diets accordingly. Prescribing diets that seem to lower LDL based on studies in healthy, insulin-sensitive people isn’t going to achieve much for the insulin-resistant who are most at risk, especially if these are still high carb, fat-phobic diets. At the very least, people at risk should be told to cut out sugar and refined starches, the products driving their insulin and triglycerides.
Whichever way you look at it – whether you think low carb is best, or you just favour a real food or Mediterranean diet with less sugar and processed food – the diet advice given in these guidelines, and supposed to be passed on by every GP in the country, represents a wasted opportunity.
 Rassias G, Kestin M, Nestel PJ. Linoleic acid lowers LDL cholesterol without a proportionate displacement of saturated fatty acid. Eur J Clin Nutr. 1991 Jun;45(6):315-20.
 Ronald P Mensink, Peter L Zock, Arnold DM Kester, Martijn B Katan; Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, The American Journal of Clinical Nutrition, Volume 77, Issue 5, 1 May 2003, Pages 1146–1155, https://doi.org/10.1093/ajcn/77.5.1146
 Farvid MS, Ding M, Pan A, et al. Dietary Linoleic Acid and Risk of Coronary Heart Disease: A Systematic Review and Meta-Analysis of Prospective Cohort Studies. Circulation. 2014;130(18):1568-1578. doi:10.1161/CIRCULATIONAHA.114.010236. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334131/
 Michael Lefevre, Catherine M Champagne, Richard T Tulley, Jennifer C Rood, Marlene M Most; Individual variability in cardiovascular disease risk factor responses to low-fat and low-saturated-fat diets in men: body mass index, adiposity, and insulin resistance predict changes in LDL cholesterol, The American Journal of Clinical Nutrition, Volume 82, Issue 5, 1 November 2005, Pages 957–963, https://doi.org/10.1093/ajcn/82.5.957
 Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams, Amy L. McKenzie, Kevin D. Ballard, Wayne W. Campbell, James P. McCarter, Stephen D. Phinney and Jeff S. Volek.
Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study.
Cardiovascular Diabetology. 2018; 17:56 https://doi.org/10.1186/s12933-018-0698-8
 Gregory A Nichols, Sephy Philip, Kristi Reynolds, Craig B Granowitz, Sergio Fazio; Increased Cardiovascular Risk in Hypertriglyceridemic Patients with Statin-Controlled LDL Cholesterol, The Journal of Clinical Endocrinology & Metabolism, https://doi.org/10.1210/jc.2018-00470
 Bartlett J, Predazzi IM, Williams SM, et al. Is Isolated Low HDL-C a CVD Risk Factor?: New Insights from the Framingham Offspring Study. Circulation Cardiovascular quality and outcomes. 2016;9(3):206-212. doi:10.1161/CIRCOUTCOMES.115.002436. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871717/
 Ballantyne CM, Olsson AG, Cook TJ, Mercuri MF, Pedersen TR, Kjekshus J. Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S.
Circulation. 2001 Dec 18;104(25):3046-51. http://circ.ahajournals.org/content/104/25/3046
 Han BH, Sutin D, Williamson JD, Davis BR, Piller LB, Pervin H, Pressel SL, Blaum CS; ALLHAT Collaborative Research Group. Effect of Statin Treatment vs Usual Care on Primary Cardiovascular Prevention Among Older Adults: The ALLHAT-LLT Randomized Clinical Trial. JAMA Intern Med. 2017 Jul 1;177(7):955-965. doi: 10.1001/jamainternmed.2017.1442.
 Lloyd SM, Stott DJ, de Craen AJM, et al. Long-Term Effects of Statin Treatment in Elderly People: Extended Follow-Up of the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER). Kiechl S, ed. PLoS ONE. 2013;8(9):e72642. doi:10.1371/journal.pone.0072642.
 Paul M Ridker, Eva Lonn, Nina P. Paynter, Robert Glynn, Salim Yusuf. Primary Prevention With Statin Therapy in the Elderly: New Meta-Analyses From the Contemporary JUPITER and HOPE-3 Randomized Trials. Circulation. 2017;135:1979-1981. https://doi.org/10.1161/CIRCULATIONAHA.117.028271
 Bathum L, Depont Christensen R, Engers Pedersen L, Lyngsie Pedersen P, Larsen J, Nexøe J. Association of lipoprotein levels with mortality in subjects aged 50 + without previous diabetes or cardiovascular disease: A population-based register study. Scandinavian Journal of Primary Health Care. 2013;31(3):172-180. doi:10.3109/02813432.2013.824157. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3750440/
Our health system is awesome at fixing up sickness, if I have an accident or get an infectious disease, get ear ache or a sore tooth, then it’s good to know that we have world class medical professionals and a system to deal with all of that.
But, let’s face it, our health system is not so awesome at preventing us getting sick, and providing us with the tools to have a great life where we are the best we can be.
Let’s face it, we spend billions on sickness and very little on health.
Let’s face it, we need to change medicine.
I’m a big fan of what has been achieved in medicine. We stand on the shoulders of giants in so many ways – Louis Pasteur, Florence Nightingale, Marie Curie, Joseph Lister, Otto Warburg, Watson and Cricks….
We’ve come so far, but each change has been painful and slow.
It took more than 50 years to move on the evidence that smoking kills to doing something about it. It took about the same time for the evidence that asbestos caused lung cancer to doing something about it. Also, in 1846, Hungarian doctor Ignaz Semmelweis found that hand washing after autopsy of dead mothers reduced neonatal death from sepsis 9-fold. He never got to see his breakthrough as he was ostracised, institutionalised, and in a twist of fate died himself of sepsis.
The time has come for change. Nutrition as medicine is a no brainer. The evidence is already there.
What’s different this time is that we have the crowd. Just like the consumer is demanding a change in regard to single-use plastic bags so to is the consumer now beginning to ask for change in the medical arena. We expect our doctors to understand nutrition and lifestyle medicine. So #letschangemedicine. We don’t have to wait for another 50 years.
Here’s what to do:
Step 1: Watch this TedX talk on the video below – just out by NZ researcher Julia Rucklidge on nutrition and mental health. It’s a game changer.
Step 2: Start making a noise yourself. People want to listen, they will follow!
Step 3: Stand by, we’ve got some bigger announcements coming in the next couple of weeks about how we are going to contribute to #letschangemedicine
It’s out! I’m honoured to be part of an authorship team with Prof Robert Lustig and Cardiologist Dr Aseem Malhotra, two rock stars of nutritional science and public health. These two guys are driving change and challenging dogma.
“Three international obesity experts, NHS Consultant Cardiologist Dr Aseem Malhotra, Professor Robert Lustig of the University of California San Francisco and Professor Grant Schofield, Auckland University of Technology have authored the most comprehensive up to date report on the science of sugar with an eight-point plan that if implemented will result in a reversal in the epidemic of type 2 diabetes within 3 years.
We have particularly focused on the tactics of the food industry, acting in the same way as Big Tobacco does. We are calling out The US Academy of Nutrition and Dietetics, British Dietetic Association (BDA), and the Dietitians’ Association of Australia who all receive annual contributions from the food industry.
Here’s our eight-point plan, all of which are evidence based to reduce population sugar consumption, and all of which were successful in curbing tobacco use.
Education for the public should emphasise that there is no biological need or nutritional value of added sugar. Industry should be forced to label added and free sugars on food products in teaspoons rather than grams, which will make it easier to understand. GS comment: We need a better food labelling system and all free sugars should be included in this. It should be obvious to the consumer how much sugar there is in products.
There should be a complete ban of companies associated with sugary products from sponsoring sporting events. We encourage celebrities in the entertainment industry and sporting role models (as Indian cricketer Virat Kohli and American basketballer Stephan Curry have already done) to publicly dissociate themselves from sugary product endorsement. GS comment: Like alcohol and tobacco in sport, the tide has turned and the untrue associations between sporting success and sugar are no longer tolerable to society. The gig’s up Big Sugar!
We call for a ban on loss leading in supermarkets, and running end-of-aisle loss leading on sugary and junk foods and drinks. GS comment: Supermarkets in New Zealand can’t loss lead on tobacco and alcohol, just add sugary drinks and junk food as well.
Sugary drinks taxes should extend to sugary foods as well. GS comment: NZ needs to join the club on sugary drink taxes, but if we want to change the three As (affordability, accessibility, and accessibility) then this tax must also extend to other junk foods. We could use the money for public health. Of our billions spent on health, the fact is most of it goes on sickness.
We call for a complete ban of all sugary drink advertising (including fruit juice) on TV and internet demand services. GS comment: As above, like tobacco and alcohol the tide has turned. Big sugar should be on notice.
We recommend the discontinuing all governmental food subsidies, especially commodity crops such as sugar, which contribute to health detriments. These subsidies distort the market, and increase the costs of non-subsidised crops, making them unaffordable for many. No industry should be provided a subsidy for hurting people. GS comment: Why do some counties make sugar cheaper yet healthy real food is costly. Sugar=wrong thing to subsidise.
Policy should prevent all dietetic organisations from accepting money or endorsing companies that market processed foods. If they do, they cannot be allowed to claim their dietary advice is independent. GS comment: Let’s save these guys because they clearly can’t identify that taking food industry money is a serious conflict of interest and undermines their credibility.
We recommend splitting healthy eating and physical activity as separate and independent public health goals. We strongly recommend avoiding sedentary lifestyles through promotion of physical activity to prevent chronic disease for all ages and sizes, because “you can’t outrun a bad diet”. However, physical (in)activity is often conflated as an alternative solution to obesity on a simple energy in and out equation. The evidence for this approach is weak. This approach necessarily ignores the metabolic complexity and unnecessarily pitches two independently healthy behaviours against each other on just one poor health outcome (obesity). The issue of relieving the burden of nutrition-related disease needs to improve diet, not physical activity. GS comment: Being fit is really good for you, but unfortunately big food is using it to confuse us about the solution to nutritional-related disease. Let’s treat these two things as important and separate, not run them against one another.
The retrospective econometric analysis and prospective Markov modelling both predict that the prevalence of type 2 diabetes will start to reduce three years after implementing these measures. This calamity has been 40 years in the making — three years is not too long to wait!
Here’s some great expert reaction so far….
“The science against sugar, alone, is insufficient in tackling the obesity and type 2 diabetes crises — we must also overcome opposition from vested interests”
Martin McKee, Professor of European Public HealthLondon School of Hygiene and Tropical Medicine said, “We now know how Big Tobacco works, pushing products that kill millions. This paper makes a compelling case that Big Food is doing the same. Maybe these corporations don’t care how they are seen. But if they do care about their reputation, then this paper shows that they have a lot to do to clean up their act.”
Tim Lang, Professor of Food Policy, City University of London, Centre of Food Policy said, “This is an important paper with fair but firm recommendations. Slowly but surely, evidence and awareness are growing that a fundamental change is needed to national and international food policies. Food manufacturing has sweetened diets unnecessarily. Influence is bought by funding arms-length organisations who take the money and cloak themselves in spurious arguments on consumer freedom. Actually, the public worldwide is conned. The impression is given that a tweak here or there will sort out obesity and the runaway non-communicable disease toll. Media ought to realise they give airtime and space to what are effectively anti public health fronts. Declaration of funding should be made before airtime is given.”
Simon Capewell, Professor of Clinical Epidemiology Department of Public Health and Policy, University of Liverpool said, “BigSugar, Big Tobacco and Big Food all use the same HARMS tactics to deny culpability: H Heaps money for politicians, journalists & scientists
H Heaps money for politicians, journalists & scientists
A Attack PH opponents & groups
R Recruit cronies
S Substitute ineffective interventions.
Simon Chapman, Emeritus Professor, Sydney School of Public Health University of Sydney, AUSTRALIA said, “The 2005 satirical movie Thank you for smoking featured a triumvirate of tobacco, alcohol and firearms lobbyists, sharing their strategies at weekly meetings they call The MOD Squad (Merchants of Death). If the movie was remade today, a fourth member from Big Sugar would be mandatory.
These modern chronic disease vectors all use the same playbook. If you want to control malaria, it’s essential you control mosquitos. If you want to control obesity, diabetes and cardiovascular disease, you must control the mosquito’s equivalent – the food industry”
Patti Rundall OBE, Policy Director of Baby Milk Action said, “A key tactic used by the food industry and all industries whose harmful practices should be regulated, is to create ‘front groups’ that represent their interest while sponsoring individuals in positions of influence – especially health professionals or anyone holding a position of trust. This allows them to secretly hijack the political and legislative process; manipulate public opinion and appear respectable. Since 1996, eight world Health Assembly Resolutions have called for conflict of Interest safeguards for those working in infant and young child feeding. These safeguards need to be implemented and extended to all those providing nutrition advice – transparency is an essential first step.”
After a big year of research, writing, and testing of our low-carb fasting method – “Super fasting” we are finally good to go.
We are super excited about What the Fast!, and how it continues the challenge on conventional nutritional-science wisdom. We’ve wrapped up the latest science, practice and yum recipes to provide you with a brilliant structure to mange your eating week (the sub-title is “How Monday and Tuesday will change your life”).
I really want to take the opportunity to thank the team, especially my co-authors Dr Caryn Zinn (aka the Whole Food Dietitian) and Craig Rodger (aka The Michelin-trained Chef), as well as Blackwell and Ruth our publishing partners.
If you have a spare 30 mins, then you might want to go to 1.03 on the fitter podcast. An interview closing sport performance, low carb, and fasting – especially concentrating on our soon to be released book “What the Fast”
You might have noticed claims in the media in the last few days that
New research conducted by Deloitte Access Economics and Nutrition Research Australia shows that if every New Zealand adult adds three serves of high fibre grain food to their daily diet, it could save the economy an estimated $607 million a year in reduced healthcare costs and lost productivity, and potentially avert 34,000 new cases of cardiovascular disease and 68,000 new cases of type 2 diabetes.
This is from a report (dae-nz-fibre-economics) that Deloitte produced for Kellogg’s. Industry funding was a conflict of interest properly reported by media. We have a rough rule of thumb around this – when industry funds basic research in labs – experiments – that’s not necessarily a bad thing, because science always needs funding, and we want answers to questions. When industry funds reviews and modelling, these are more likely to be subject to cherry-picking to favour the sponsor – they are questions of interpretation, so the risk of bias is higher.
The causes of disease and mortality that grain fibre is supposed to be able to prevent are cardiovascular disease and type 2 diabetes.
Based on data from published meta-analyses, the number of cases averted was estimated by assuming that a one-gram increase in grain fibre reduces the risk of CVD by 1.1% and T2D by 2.5% (Threapleton, 2013; InterAct Consortium, 2015).
We took a closer look at the evidence used to calculate the larger of the two benefits, that for type 2 diabetes. This was the EPIC-InterAct study and meta-analysis; the EPIC-InterAct study was a multicentre European observational study that didn’t find a protective association for grain fibre once adjusted for BMI (but there are some interesting details we’ll discuss later), so the authors added a meta-analysis (a statistical method that pools all available studies world-wide) that did find a protective association with grain fibre.
“However, the findings from our updated meta-analysis of prospective studies do support an inverse association between total fibre and cereal fibre intake and risk of type 2 diabetes, with a 9% and 25% lower RR per 10 g/day, respectively, independent of BMI.”
So an extra 10g of grain fibre reduces your risk of type 2 diabetes by 25%. Or does it? Actually, it depends on where you live.
There are many countries in EPIC-Interact without a protective association between grain fibre and type 2 diabetes, including France with a non-significant HR of 1.72 (that’s 72% worse). Another exception is the UK with a non-significant HR of 0.74 (26% better).
What are the differences in these populations? The French cohorts, for some reason, are all 100% female, which isn’t the case for any other country. And the largest of the two UK cohorts is EPIC-Oxford. “The majority of participants recruited by the EPIC Oxford (UK) centre consisted of vegetarian and “health conscious” volunteers from England, Wales, Scotland, and Northern Ireland”. So these health conscious volunteers are probably being compared with people with lower fibre intakes in the less health-conscious UK cohort.
Sweden always interests us because one of their two cohorts is the Malmö Diet and Cancer Study, which unlike the usual observational diet studies in this, or any other meta-analysis, uses the more accurate 7-day food diary for all subjects, and in Sweden the HR is a more reasonable 0.96. So less confounding by conscientiousness and more accurate diet recall tends to minimize the cereal fibre and type 2 diabetes association. If cereal fibre prevented type 2 diabetes in any important or unique way, it should probably show up in most of these populations, not just a few.
What about the other countries in the meta-analysis? Most of the weighty studies in favour of fibre for type 2 diabetes prevention in the EPIC-Interact meta-analysis come from the USA. There are two important facts about the USA – low fibre intakes are lower than they are anywhere else (so basically a high intake of deep fried food, white breads, and sweetened soda in these low-fibre groups), and conscientiousness is an identifiable confounding factor in many populations. For example, the Nurses’ Health Study and Health Professionals’ Follow-up Study; here we have the populations not only given the most advice about fibre being healthy, but also given the job of passing it on to the other US populations. In other words, grain fibre – like red meat – is one of the signifiers separating conscientious Americans from other Americans (it’s harder to eat fruit and vegetables without their fibre, and vegetables in the US includes fried potatoes). It’s almost a class distinction.
Closer to home, there are 3 Australian studies, two small ones with protective associations between grain fibre and type 2 diabetes (smaller studies have less weight in a meta-analysis) and a large one, Hodge 2004, with none. However Hodge 2004 finds that white bread is associated with type 2 diabetes, and that lower GI carbs, including sugar, aren’t.
White bread in Australia is so bad that even sugar looks good by comparison.
Does it follow that putting a few grams of bran in white bread will make it safe, or even good for you? Why not just say “avoid white bread”? This would definitely be our advice! Anyway, if fibre isn’t associated with type 2 diabetes in a fairly large sample of Australians, who tend to have fairly high fibre intakes anyway (by OECD standards), do Kiwis still need to take their lead from the USA?
“The mean±SD fibre intake in the [European] subcohort was 22.9± 6.2 g/day (ranging from 19.9 g/day in Sweden to 25.2 g/day in Denmark; data not shown).”
These figures for European countries are very similar to the averages for New Zealand – 22.8 g/day for men and 17.9 g/day for women.
Germany (7.40%) and Denmark (7.20%) have higher diabetes prevalence rates than Sweden (4.70%). USA’s mean total fibre intake is 16.1 g/day and diabetes prevalence is 10.80%. This would suggest that there is a suboptimal fibre intake, or perhaps just a protective effect of the real food, higher fat diets eaten in a place like Sweden, where (in Malmö) dairy fat has a protective association with type 2 diabetes, total fat has a protective association with CVD mortality in men, and fibre is protective against heart attacks only in combination with saturated fat (most of this is grain fibre in Malmö, probably from rye bread).[4,5] Sucrose – sugar – is the only nutrient/food/ingredient significantly associated with increased heart disease risk in Malmö. Its effect on the lipid profile is to increase triglycerides.
Participants who consumed >15 % of their energy intake (E%) from sucrose showed a 37 (95 % CI 13, 66) % increased risk of a coronary event compared with the lowest sucrose consumers (<5 E%) after adjusting for potential confounders. The association was not modified by the selected lifestyle factors.
There are no nutrients unique to grains. But some grain fibres, especially oat bran, are a very good source of silicon, a mineral which might be more important for cardiovascular health than is currently recognised. Other good sources of silicon are mineral water (the higher the total dissolved solids, the higher the silicon content is likely to be), green beans (especially) and other crunchy fibrous vegetables, bone broth, red wine and beer, and some herb teas, especially horsetail, oatstraw, and nettle. Oat bran is low in digestible carbohydrate and could definitely be included in the LCHF diet if anyone thought this necessary (it makes a great binder for mince patties).
The push from Kelloggs is to increase fibre by eating more grains and cereals – this is conflating any benefit of fibre with the effect of starch (and sugar if we’re talking breakfast cereals). Indeed fibre might be healthful but if you get it by adding extra bread and breakfast cereal what does that mean? for example, from EPIC-Netherlands:
Dietary GL was associated with an increased diabetes risk after adjustment for age, sex, established diabetes risk factors, and dietary factors [hazard ratio (HR) per SD increase: 1.27; 95% CI: 1.11, 1.44; P < 0.001] [corrected]. GI tended to increase diabetes risk (HR: 1.08; 95% CI: 1.00, 1.17; P = 0.05). Dietary fiber was inversely associated with diabetes risk (HR: 0.92; 95% CI: 0.85, 0.99; P < 0.05), whereas carbohydrate intake was associated with increased diabetes risk (HR: 1.15; 95% CI: 1.01, 1.32; P < 0.05). Of the carbohydrate subtypes, only starch was related to increased diabetes risk [HR: 1.25 (1.07, 1.46), P < 0.05]. All associations became slightly stronger after exclusion of energy misreporters.
And don’t forget the PURE study, as well as the Czech ecological analyses (below) – there are protective effects from moderate amounts of high fibre foods, but replacing fat with lots of carbohydrate is overall associated with a worsened metabolic profile and higher mortality.[10, 11]
The aim of this study was a large-scale ecological analysis of nutritional and other environmental factors potentially associated with the incidence of cardiovascular diseases (CVDs) in the global context. Indicators of CVDs from 158 countries were compared with the statistics of mean intake (supply) of 60 food items between 1993 and 2011, obesity rates, health expenditure and life expectancy. This comparison shows that the relationship between CVD indicators (raised blood pressure, CVD mortality, raised blood glucose) and independent variables in the global context is influenced by various factors such as short life expectancy, religiously conditioned dietary customs, the imprecision of some statistics and undernutrition. However, regardless of the statistical method used, the results always show very similar trends and identify high carbohydrate consumption (mainly in the form of cereals and wheat in particular) as a dietary factor most consistently associated with the risk of CVDs. These findings are in line with the changing view of the causes of CVDs.
From this evidence, it might be better to get the fibre from the low-starch foods; but if you do eat grains (not everyone is or needs to be low-carb), eating only whole grains, i.e. grains that you can see are whole or minimally broken, in relatively small amounts, and avoiding refined grains as far as possible is the pattern associated with most benefit.
The Bottom line: there are almost certainly people at higher risk of type 2 diabetes and cardiovascular disease because their diets are too dependent on refined and processed carbohydrate foods, especially sugars and grains. Their risk would indeed be lower if they replaced these with whole grains – brown rice, barley, oats and so on. This may be due in part to the fibre content, but it may also be due to the slower release of glucose and thus healthier insulin response to a grain when it hasn’t been powdered; fibre in a powdered grain doesn’t do much to reduce its impact. Yer dreamin if you think that just adding bran to processed carbs – which is what Kellogg’s products do – is going to make an impact on disease rates. Eating whole foods instead of food products might give us a chance.
For people with carbohydrate intolerance, grains are too carbohydrate-dense a food to consume in any quantity, but other fibre-rich foods are available to substitute.
However, to say that high-fibre diets are better is a generalisation – the benefits of fibre require the cooperation of gut bacteria and the gut, and quite a few people who look to diet to improve their health find that lower-fibre diets such as FODMAP exclusion diets and occasionally even zero-carb carnivore diets give significant improvement where high-fibre diets fail.
The What The Fat? diet is high-fibre because fibre increases satiety and there is some evidence for other health benefits, but fibre isn’t necessarily something there should be a bulk ruling about.
P.S. Ironically, when the Herald ran a news story on the Deloitte/Kellogg’s report, the high fibre success story they spoke to was a low(er) carber! There are only a couple of slices of brown bread in this story.
 The InterAct Consortium. Dietary fibre and incidence of type 2 diabetes in eight European countries: the EPIC-InterAct Study and a meta-analysis of prospective studies. Diabetologia. 2015;58(7):1394-1408. doi:10.1007/s00125-015-3585-9.ghb https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4472947/
 The InterAct Consortium, Langenberg C, Sharp S, et al. The InterAct Project: An Examination of the Interaction of Genetic and Lifestyle Factors on the Incidence of Type 2 Diabetes in the EPIC Study. Diabetologia. 2011;54(9):2272-2282. doi:10.1007/s00125-011-2182-9.
 Hodge AM, English DR, O’Dea K, Giles GG. Glycemic index and dietary fiber and the risk of type 2 diabetes. Diabetes Care. 2004;27:2701–2706. doi: 10.2337/diacare.27.11.2701
 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. Obukhov AG, ed. PLoS ONE. 2012;7(2):e31637. doi:10.1371/journal.pone.0031637
 Leosdottir M, Nilsson PM, Nilsson JA, Månsson H, Berglund G. Dietary fat intake and early mortality patterns–data from The Malmö Diet and Cancer Study. J Intern Med. 2005 Aug;258(2):153-65. link
 Warfa K, Drake I, Wallström P, Engström G, Sonestedt E. Association between sucrose intake and acute coronary event risk and effect modification by lifestyle factors: Malmö Diet and Cancer Cohort Study. Br J Nutr. 2016 Nov;116(9):1611-1620. Epub 2016 Oct 24.
 Sonestedt E, Hellstrand S, Schulz C-A, et al. The Association between Carbohydrate-Rich Foods and Risk of Cardiovascular Disease Is Not Modified by Genetic Susceptibility to Dyslipidemia as Determined by 80 Validated Variants. Müller M, ed. PLoS ONE. 2015;10(4):e0126104. doi:10.1371/journal.pone.0126104.
 Loeper J, et al. Study of fatty acids in atheroma induced in rabbits by an atherogenic diet with or without silicon IV treatment . Life Sciences 1988, 42:2105-2112.
 Sluijs I, van der Schouw YT, van der A DL, Spijkerman AM, Hu FB, Grobbee DE, Beulens JW. Carbohydrate quantity and quality and risk of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) study. Am J Clin Nutr. 2010 Oct;92(4):905-11. doi: 10.3945/ajcn.2010.29620. Epub 2010 Aug 4.
 Dehghan M, Mente A2, Zhang X, et al. Prospective Urban Rural Epidemiology (PURE) study investigators. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062. doi: 10.1016/S0140-6736(17)32252-3. Epub 2017 Aug 29.
 Grasgruber P, Cacek J, Hrazdíra E, Hřebíčková S, Sebera M. Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries. Preprints 2018, 2018020066 (doi: 10.20944/preprints201802.0066.v1). https://www.preprints.org/manuscript/201802.0066/v1