Here’s a little piece I wrote for the Education sector in the Education Gazette, around the big issues for our kids..

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.[1] 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.[2] 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).[3]

A survey of patients with anorexia nervosa found that vegetarians and vegans were over-represented and were more likely to have a persistent condition.[4]

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, P_trend=0.006) for dietary insulin load and 1.66 (95% CI: 1.10-2.50, P_trend=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, P_trend=0.03) for dietary insulin load and 1.32 (95% CI: 1.02-1.71, P_trend=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 (P_interaction=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.

References

[1] 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.

[2] 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.
https://linkinghub.elsevier.com/retrieve/pii/S0165-0327(16)32391-6

[3] 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

https://onlinelibrary.wiley.com/doi/abs/10.1111/acer.13494

[4] 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.

[5] 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.

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.

Enjoy

Cardiovascular Disease Risk Assessment and Management for Primary Care.
https://www.health.govt.nz/system/files/documents/publications/cvd-risk-assessment-and-management-for-primary-care-v2.pdf

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.

They say……

“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.[1]

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.[2]

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.[3]

“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.[4]

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.[5]

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.[6]

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.[7]

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.[8]
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).

4S – Open squares are highest TG/ lowest HDL quartile on statin, closed squares on placebo. Open circles are lowest TG/ highest HDL quartile on statin, closed circles on placebo.

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.[9]

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.[10]

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.[11]

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.[12]

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.

References

[1] 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.

[2] 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

[3] 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/

[4] 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

[5] 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

[6] 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

[7] 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/

[8] 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

[9] 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.

[10] 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.

[11] 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

[12] 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/

Hi everyone,

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.

I really hope you like it.

The book is available for pre-order now at whatthefatbook.com

There is a limited initial print run available and we expect this will sell out.

The kindle version is also available for preorder.

Thanks again everyone for all your support, its been quite a journey over the last few years.

Grant Schofield
Professor of Public Health
Director Human Potential Centre
AUT University

The whole range!

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”

https://www.fitter.co.nz/fitter-radio/2018/4/8/episode-208-prof-grant-schofield