This is well worth the watch. Some NZ twists in here from our team and the battles going on (see the last post for more on the spoiler plays against low carb and diabetes reversal coming out of NZ that were mentioned by Aseem)
We were surprised to hear this Radio New Zealand interview with Jim Mann regarding a Chinese study he co-authored. In it he predicts various terrible things for people eating LCHF diets, which we think is out of line and not supported by the study.
In fact, the LCHF and Paleo community have been warning about exactly the type of diet that was used in the study – high in energy from soybean oil, rice, and wheat – for years, and Jim Mann’s crowd have attacked us for that, while the NZ Ministry of Health and Heart Foundation they advise has actively promoted such a diet. So it’s ironic that, as soon as we’re proved right, this is presented as evidence against our own, quite different advice – rather than being acknowledged as the humbling result it is for those supporting the current guidelines.
“Of particular interest was what happened to the bacterial flora of the gut, the microbiome underwent radical changes in these three different groups.
The low fat group had a bacterial profile which was compatible with low risk of a number of western diseases: heart disease and cancer.
The high fat group had a very different profile of bacteria in their gut, one more compatible with an increased risk of bowel cancer and also a much higher risk of inflammation leading to cardiovascular disease, heart disease and possibly diabetes,” Prof Mann says.
The results, he says, were “pretty scary.”
“It’s a strong message for what is happening in China, but I believe also a strong message for New Zealand and other similar countries where at least some people believe there are benefits to a high fat diet.”
All three groups had consistent and similar intake of vegetables, he says.
“A lot of people have argued you can have a high fat diet as long as you have a lot of veggies, I think that’s a serious misapprehension. If you are having a really high fat diet you’re not going to get a high fibre diet at the level of fibre that will be protective against these diseases.”
So what was the study?
“In a 6-month randomised controlled-feeding trial, 217 healthy young adults (aged 18–35 years; body mass index <28 kg/m2; 52% women) who completed the whole trial were included. All the foods were provided during the intervention period. The three isocaloric diets were: a lower-fat diet (fat 20% energy), a moderate-fat diet (fat 30% energy) and a higher-fat diet (fat 40% energy). The effects of the dietary interventions on the gut microbiota, faecal metabolomics and plasma inflammatory factors were investigated.”
The most important part of the paper is this statement:
Notably, the predicted lipopolysaccharide biosynthesis and arachidonic acid metabolism pathways were also increased in response to the higher-fat diet. Lipopolysaccharide is known to induce the release of arachidonic acid and its inflammation-involving metabolites, such as prostaglandins, thromboxane and leukotrienes. It should be noted that the intake of polyunsaturated fatty acids (PUFAs) was relatively high in the higher-fat diet group (24% of total energy) owing to exclusive use of soybean oil, which is rich in n-6 PUFA. A higher intake of n-6 PUFA has been reported to have proinflammatory effects.
In the interview, host Jesse Mulligan, who is a chef and knows his oils, does a great job of extracting this part of the story from Prof Mann. The n-6 (omega-6) PUFA in soy and other seed oils is linoleic acid; linoleic acid is the precursor of arachidonic acid (AA) and high levels drive AA synthesis. Lipopolysaccharide is also known as endotoxin and is a product of gram-negative bacteria that stimulates an immune response if it enters the bloodstream; a little endotoxin seems to be beneficial, but a lot can drive inflammatory diseases by activating the TLR4 receptor on immune cells.
Now, the traditional Chinese diet varies across regions so that it is hard to generalise, but the low fat Southern version looks like this – lots of green and coloured vegetables ( a very wide diversity, not just a large quantity), nose-to-tail meat (mostly pork and chicken), eggs, legumes, and white rice. Though low in fat, it can be relatively high in cholesterol due to the use of organ meats. Cooking can be by steaming, or stir-frying using small amounts of various oils. The dietary transition has seen more deep-frying in oils and the use of more oils in processed foods. Most of this is soybean oil (the majority of the soy grown in the former Amazon rainforest is now exported to China where it is used to make oil and soy protein, some of which is no doubt exported to NZ and the Pacific).
The equivalent of a 40% seed oil diet in NZ would be deep fried meals from KFC, plus Best Foods mayonnaise – popular foods in the more deprived areas of NZ.
Now, why would a high fat diet be bad for the microbiome? A moment’s thought will show that this doesn’t make sense as a generalisation. The microbiome is established in infancy, starting with birth when bacteria are transferred from the mother. The diet in infancy for mammals is, by definition, milk, a food always high in saturated fat and low in polyunsaturated fat. At day 16, human breast milk is 54% fat; of this fat 44.6% is saturated, 37.6% is monounsaturated, 14.6% is polyunsaturated omega-6 and 3.1% is omega-3. in hunter-gatherer populations without access to seed oils the omega-6 content is lower – e.g. 10% in the Tsimane of Bolivia vs 18% in the population of Cincinnati, USA.
Breast milk contains small amounts of soluble fibre, and lactose which lactobacillus can ferment but which is mostly absorbed and used for energy and growth.
However – lactobacillus also metabolise saturated fats. And some lactobacillus species make saturated fats that many other bacteria rely on between meals – these are the odd-chain fatty acids, C15 and C17, which you’ll find in dairy, beef, and lamb fat, but other dietary saturated fats can substitute for C15 and C17 when their production is disrupted by alcohol.
Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis* and reduces ethanol-induced liver injury in mice.
(*Eubiotics (Greek eu = good/healthy, bios = life) is the science of hygienic/healthy living. The term is used in the feed industry where it refers to a healthy balance of the microbiota in the gastrointestinal tract.)
And really, this should be obvious – if you buy yoghurt, the original probiotic food, you will only find two types to choose from – that made from milk (the animal food highest in saturated fat), and the vegan yoghurt made from coconut (the plant food highest in saturated fat).
Don’t blame the butter for what the soyabean did.
It has been known since 1945 that polyunsaturated fatty acids are toxic to lactobacillus and other gram-positive bacteria. In the China trial, the high soybean diet decreased levels of the gram-positive bacteria, Faecalibacterium, and increased levels of the gram-negative bacteria Bacteroides and Alistipes. A 2018 review  stated that:
Linoleic acid and the other two major unsaturated FAs in SBO, oleic acid (18:1), and alpha-linolenic acid (18:3), are known to be bacteriostatic and/or bactericidal to small intestinal bacteria as non-esterified (free) fatty acids in vitro at concentrations found in the small intestine (Kabara et al., 1972; Kankaanpää et al., 2001; Kodicek, 1945; Nieman, 1954). The primary modes of killing include permeabilization of cell membranes (Greenway and Dyke, 1979) and interference with FA metabolism (Zheng et al., 2005). Affected microbes are predominantly Gram-positive bacteria including the genus Lactobacillus (Nieman, 1954). Lactobacilli are particularly important as they are considered beneficial members of the human small intestine (Walsh et al., 2008; Walter et al., 2007; Walter et al., 2011). They have been shown to be growth inhibited by the specific FAs present in SBO (Boyaval et al., 1995; De Weirdt et al., 2013; Jenkins and Courtney, 2003; Jiang et al., 1998; Kabara et al., 1972; Kankaanpää et al., 2001; Kodicek, 1945; Raychowdhury et al., 1985). It is interesting to note that the human-associated L. reuteri underwent a population bottleneck that coincides with the increase in SBO consumption in the U.S. and is far less prevalent than it was in the past (Walter et al., 2011). In the 1960’s and 1970’s prior to the emergence of SBO as a major dietary fat source, L. reuteri was recovered from the intestinal tract of 50% of subjects surveyed and was considered a dominant Lactobacillus species of the human gut (Reuter, 2001). Today, however, it is found in less than 10% of humans in the USA and Europe (Molin et al., 1993; Qin et al., 2010; Walter et al., 2011), yet it is present at a reported 100% prevalence in rural Papua New Guineans (Martínez et al., 2015).
Yet the paper Jim Mann co-authored cites none of this research. There is only one reference in it (46) to the possibility that a high omega-6 intake can be inflammatory, and this review does not mention the effect on the microbiome – despite being written by microbiologists.
This sort of thing is all-too common – a lack of curiosity in nutrition research. To plan an experiment like the Chinese soybean oil trial takes years. If you’re planning to feed an unusual amount of linoleic acid – 24% of energy – to people and measure its effects on the microbiome, why are you not curious enough to search for the evidence about the effect of linoleic acid on the microbiome? If you think more fat is bad fat, whatever its composition, you might miss this step. It’s possible that reference 46 and the comment about linoleic acid was added by a reviewer and was not even part of the paper as originally submitted. Or, it might have been included by Jim Mann, who is not a complete fool and who has long been exposed to Paleo arguments about omega-6, but went over the heads of his coauthors, the microbiologists.
So the microbiome results are no surprise to us (though predicting disease from the microbiome at our present stage of knowledge would be about as reliable as predicting it from tea leaves or tarot cards, gram-positive lactobacillus and bifidus probiotics have been well-tested and are for example associated with a reduction in rehospitalization for mania in bipolar disorder, HR 0.26, 95% confidence interval [CI] 0.10, .69; P = .007).
But what is surprising, and should have surprised Jim Mann, is that LDL cholesterol did not go down on the high-PUFA diet. After all, the effect of PUFA on cholesterol has been the excuse for promoting these oils. There is increasing doubt about whether the effects of fat (amount or type) on LDL cholesterol counts has any important influence on CVD risk in the first place, but the news that soybean oil has no effect on LDL in a real world experiment means that there is no longer any rationale for recommending it.
So come on. This isn’t good interpretation of the results. The results of this high-soybean oil study say nothing about the effects of high fat diets when those fats are traditional fats that are not toxic to beneficial bacteria. The results of this study, where more energy came from carbs (mainly wheat and rice) than from fat, can say nothing about LCHF diets where wheat and rice are avoided or limited. Jim Mann’s comments about “the level of fibre that will be protective against these diseases” are based on epidemiology where very high levels of fibre are associated, not with IBD as in the real world, but with protection against all sorts of diseases. But we have news for him – very high levels of linoleic acid were also protective in epidemiology. Just not in the real world. The majority of associational results discovered in epidemiology are not borne out by later experiments, because associational epidemiology is inherently inaccurate, and can reflect the bias of epidemiologists, who are today also influencers of the populations they study.
Postscript: The results of this study can help us to understand one of the more interesting nutritional epidemiology papers. The Malmo Diet and Cancer Study (MDCS) is a large cohort study that uses a 7-day food diary to collect data and also has stricter validation criteria than FFQ research, putting it into the highest category of evidence for such studies. In the MDCS, of 8,139 male and 12,535 female participants (aged 44–73 y), there were 1,089 male and 687 female iCVD cases (Ischemic cardiovascular disease, including strokes and heart attacks) during a mean 13.5 year follow-up. That’s about 1 in 8 men and 1 in 20 women. For iCVD, after full adjustment, fiber intake was negatively and significantly associated with iCVD in women (24 percent lower risk in the highest intake quintile compared to the lowest, 95 percent confidence interval −3 to −41 percent, p for trend = 0.022), but no other significant associations were noted, except a borderline (p=0.050) protective association of fibre with stroke for men. But here’s where it gets interesting – in the post-hoc analysis, adjusting for the other nutrients revealed that the combination of high fibre and high saturated fat was protective; that is, for men lowest quintiles of SFA and fibre combined had statistically significant HRs for iCVD of 1.82, which is pretty high, whereas high fibre/low SFA and high SFA/low fibre had the reference 1. For women, the lowest risk of iCVD, 0.36, was in the highest fibre, second highest SFA quintile, with the highest SFA highest-fibre quintiles being similar but non-significant.
This result makes sense if both fibre and saturated fats are prebiotic foods, and if the combination supports eubiosis better than the combination of fibre and unsaturated fats.
 Wan Y, Wang F, Yuan J, et al Effects of dietary fat on gut microbiota and faecal metabolites, and their relationship with cardiometabolic risk factors: a 6-month randomised controlled-feeding trial. Gut Published Online First: 19 February 2019. doi: 10.1136/gutjnl-2018-317609
 Marshall JC. Lipopolysaccharide: an endotoxin or an exogenous hormone? Clin Infect Dis. 2005 Nov 15;41 Suppl 7:S470-80.
 Jensen RG. Lipids in human milk. Lipids 1999 Dec;34(12):1243–71. http://pmid.us/10652985
 Martin MA, Lassek WD, Gaulin SJ, et al. Fatty acid composition in the mature milk of Bolivian forager-horticulturalists: controlled comparisons with a US sample. Matern Child Nutr. 2012;8(3):404-18.
 Chen P, Torralba M, Tan J, et al. Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis and reduces ethanol-induced liver injury in mice. Gastroenterology. 2014;148(1):203-214.e16.
 Kodicek E. The effect of unsaturated fatty acids on Lactobacillus helveticus and other Gram-positive micro-organisms. Biochem J. 1945;39(1):78-85.
 Di Rienzi SC, Jacobson J, Kennedy EA, et al. Resilience of small intestinal beneficial bacteria to the toxicity of soybean oil fatty acids. Elife. 2018;7:e32581. Published 2018 Mar 27. doi:10.7554/eLife.32581
 Dickerson F, Adamos M, Katsafanas E. Adjunctive probiotic microorganisms to prevent rehospitalization in patients with acute mania: A randomized controlled trial.
Bipolar Disord. 2018 Nov;20(7):614-621. doi: 10.1111/bdi.12652. Epub 2018 Apr 25.
 Ioannidis JPA. The Challenge of Reforming Nutritional Epidemiologic Research. JAMA. 2018;320(10):969–970. doi:10.1001/jama.2018.11025
 Wallström P, Sonestedt E, Hlebowicz J, et al. Dietary fiber and saturated fat intake associations with cardiovascular disease differ by sex in the Malmö Diet and Cancer Cohort: a prospective study. PLoS One. 2012;7(2):e31637.
SCIENCE IN A MINUTE: @Caryn Zinn Nutrition reviews the latest Lifestyle Medicine research released two weeks ago in the British Medical Journal (BMJ) on weight-loss maintenance.
Which diet works best for maintaining weight loss? Find out…
What’s more important to you – your left arm or your right foot? What would you rather keep if you had to lose one or the other?
Well, here’s my opinion in the video below and longer blog here
Actually it’s all about how we need to talk about fitness more. Fitness is medicine. Enjoy…and get fit!
You will see yourself linked to Prekure’s www site. Prekure – “prevention is cure” is a social enterprise I’m part of with 8 other health professionals from oncology to public health to general practice to pharmacy.
We are hoping to make a dent in medicine – to move from drugs as frontline treatment, to lifestyle as first line medicine. The social arm offers free lifestyle medicine programs which really work, available for everyone. We are also doing medical education training for health professionals – in lifestyle medicine, of course. We want to bring today’s evidence to the front line of healthcare – its compelling.
We’ve just got going. Stay tuned and please join our community to change medicine to “prevention as cure”. More to come.
Prekure’s social links below
Here’s a little piece I wrote for the Education sector in the Education Gazette, around the big issues for our kids..
Opinion piece: By Grant Schofield, Professor of Public Health and Director of the Human Potential Centre at AUT Millennium, and the Ministry of Education’s Chief Education Health and Nutrition Advisor.
What should a rich, developed country like New Zealand be aspiring towards? I think having a good life for all would be a great aspiration.
But what’s a good life?
A good life starts with having the health to physically and mentally do whatever else you want to. Without that base, you have very little to go on with.
New Zealand’s report card looks pretty poor as far as ‘good health’ is concerned. Yes, we live longer than we ever have, but our healthy life expectancy hasn’t kept up. There’s now a big gap between actual life expectancy and ‘healthy’ life expectancy. Men average 79 years of life, but just 65 of healthy life. Women average 83 years, with 66 healthy. Māori men average 72 years with just 54 years healthy.
And…we spend $18.1 billion on health. But the reality is that almost all of those billions go on sorting out sickness. That sickness system is helping us have longer lives but not necessarily better lives.
Why I am writing this in the Gazette? Shouldn’t we be focused on young people, not old people, as educators?
Well, if we want to change the behaviours that really determine our health, we are going to have to look outside the health system. And we are going to have to start with young people.
The five big things that affect our healthy life are all set up when we are young. It’s about not smoking, less alcohol, better nutrition, better sleep, and how much we move (more activity). We’ve made great progress on smoking and to an extent alcohol harm, but nutrition, sleep, and physical activity are all arguably getting worse.
A recent PISA report from the OECD tells us that exercise and activity are important for the wellbeing of our youth.
Here’s the top four challenges I think we all face in boosting our young people’s health and wellbeing, and ultimately that of society:
Challenge 1: Mobile devices
They are pretty much the most useful device invented. You carry instant access to all the knowledge of humanity in your hand. Awesome. And they are awesome tools. The mobile is a great servant, yet a hideous master.
High device use disrupts sleep quantity and quality, reduces activity, and has the potential to disrupt genuine experiences with friends, and promote bullying. Understanding how to effectively use, but contain mobile devices, in our young people is the critical challenge of our time. As parents and educators, let’s help ourselves too. Let’s model what we want to see in our youth.
Challenge 2: Getting outside
Getting outdoors and moving is effective in improving mood, reducing depression, improving academic performance, and improving sleep. This can easily be a priority in education. Scientifically it makes sense. My challenge to you is how to build this into the rest of your curriculum delivery. The Hauora aspects of the HPE curriculum lend achievements in this curriculum and learning area to also achieving across multiple other areas of literacy, numeracy and inquiry.
Can you take some of your teaching outside and have physical activity involved?
Challenge 3: Free-range kids
Risk and adventure on your own terms is part of growing healthy kids. We now know that frontal lobe development (read self-control and risk management) develops when you engage in unstable outdoor activity. That means play with consequences. Playstations do not help this development. There are no consequences when you crash your car on Grand Theft Auto. There are consequences for poor tree climbing skill.
Schools can allow tree climbing, adventurous and vigorous play, and even some full contact games. I’m not talking about negligence. I’m talking about helping children learn about risk before they are driving a car and exposed to drugs and alcohol as teenagers. We have a choice in society when we learn this. The earlier the better in my opinion.
Challenge 4: Food
It’s pretty obvious that the modern, industrial food supply bears little resemblance to what humans have eaten for most of the time we’ve been on the planet. Highly processed and packaged food is bad for the youth brain, body, learning and their mental health. There is so much infighting and confusion in nutrition science, but one thing we all agree on is that whole unprocessed food is the way to go.
That’s why I’d like to introduce you to the ‘HI’ (Human Interference) factor. The guide to healthy eating need not get into the ins and outs of fats, carbs, sugars and so on. All we need to ask ourselves is, “Was this plant/animal recently alive in nature running around or growing somewhere?” Yes = eat it. No – it doesn’t resemble anything recently alive = don’t eat it. If we can start a movement around this approach, we will be most of the way to eating healthy again. Big Food companies, who market highly processed, sugary foods won’t like this one bit. In my opinion, Big Food shouldn’t be welcome in our schools. They are behaving exactly like Big Tobacco did – creating confusion, buying science, giving misinformation, and associating themselves with sport and young athletes.
That’s it. Challenges, not answers.
Once again we have headlines about how we need to cut back on meat consumption for the sake of our health, and the planet’s, fueled by a recent review. We’ve addressed the climate effects of ruminant agriculture before, this (most particularly with regard to intensive dairying and least of all with regard to sheep) is a conversation we need to keep having in NZ, but we would prefer experts to stop conflating this agenda with health advice.
As we’ll show, no-one has good data about how much meat New Zealanders currently eat, but past figures show that large numbers of Kiwis were deficient in the very nutrients that meat supplies in goodly amounts, making overconsumption unlikely. We’ll also present evidence that meat avoidance may have serious effects, which our health authorities may be overlooking.
It is not our position that vegetarian and vegan diets are intrinsically harmful; educated people with sufficient income, or people with sound cultural support in the case of traditional vegetarian diets, are those most likely to eat nutritionally adequate diets without meat, or with little meat. But meat and other animal foods are so nutrient dense as to be dietary fail-safes for the majority of people who do not have time, inclination, money, or education to guarantee good nutrition otherwise, as we will see. Random advice to cut these foods from the diet, delivered without nuance as primetime TV News, can only harm the most vulnerable members of society.
How much meat is in our “high meat” diet?
New Zealand authorities have not calculated the amount of meat in our diets since the 2008/2009 Health and Nutrition Survey. (another survey was done since, but the only diet questions in it were about one about sugary soft drink consumption and one about getting 5+ servings of fruit and vegetables a day).
According to the 2008/2009 nutrition survey, the protein intakes estimates of New Zealanders were 16.4% and 16.5% of energy for males and females respectively, at the lower end of dietary recommendations of 15-25%.
Bread and other grain-based foods supplied nearly a third of our protein intake, only a fifth of which came from red meat, processed meat, and pork. (We calculate this as an average of only 16.5 grams of meat protein per day in a 2,000 kcal diet).
Similarly, meat contributed significantly less iron to the diet (about 13%) than bread, pasta, and breakfast cereals (29%). These figures do not indicate a population overeating meat; if anything, they seem to indicate a population overly reliant on refined wheat in all its forms (only the processed forms of grains, which are supplemented, are a good source of iron).
When these results were published in 2011, Professor Elaine Rush, Professor of Nutrition, Faculty of Health and Environmental Science, Auckland University of Technology made the following comments on the Science Media Centre blog:
The biggest whammy is for people living in more deprived areas. They are more likely to be overweight or obese, not meeting recommended micronutrient intakes such as iron, vitamin A and calcium. Bread continues to be the major contributor of energy, protein, and carbohydrate to the New Zealand diet, In comparison to white bread, light or heavy whole grain bread was chosen by 60% of the population, but almost 50% of young adults compared to 25% of older people reported eating white bread. The most socioeconomically deprived 20% were twice as likely to consume white bread compared to the most well off 20% (20% vs 40%).
The evidence is clear, in 2008 New Zealanders were not well nourished, many did not have enough money to buy nutritionally adequate and safe foods and were not healthy. Since then the economic recession and the ever-increasing cost of food mean that we are unlikely to be improving. More importantly our present children and those still to be conceived are not likely to have an optimal start to life continuing the cycle. A whole of New Zealand response is required because it is not a personal choice or responsibility- particularly for children. We produce enough good food to feed everyone well – why the gap between the farm and the mouth?
Why indeed? Our red meat exports are higher than ever, yet this seems to be diverted away from our population. Zinc seems to be very much an indicator of animal food (red meat, shellfish, and cheese) consumption in the MOH report, as no good plant sources of zinc are listed.
Nearly a quarter (24.7 percent) of New Zealanders aged 15 years and over were not getting enough of the trace element zinc in their diet, with 39.1 percent of men and 11.2 percent of women missing out. The median usual daily intake of zinc was 12.9mg for men and 9mg for women, and even lower for older people. These intakes were down on those seen in the 1997 survey.
As the RDI of zinc is 14mg per day for men and 8mg/day for women, this means that most men and almost half of women in NZ were below the RDI for zinc in 2008/2009. Hardly a population eating too much meat back then, but we don’t know if this is even worse today. And there’s the problem – experts racing off making blanket recommendations when there is insufficient data about the current position.
Adverse effects of meat avoidance – mental health.
We have serious concerns about the effect of meat avoidance at a population level as a public health-endorsed recommendation, whether the reason for it is ethical, socio-political, environmental, or flat-out poverty. Such advice needs to meet robust criteria for cause and effect, the effect needs to be strong and with little chance harm occurring with populations taking such recommendations.
The study by Hibbeln et al that found increased rates of depression in vegetarian men cites six other studies with similar findings, including two in adolescents. Only one cited study, in US Seventh Day Adventists – a relatively privileged group which plays an important role in the promotion of meat avoidance – had different results.
Another study by Hibbeln et al found that vegetarianism in pregnancy was associated with substance abuse (alcohol and cannabis) in offspring, and screening for the effect of a vitamin B12 absorption allele increased confidence that the relationship was causal (there was no association by diet in those who had genetically poor B12 absorption whatever their diet).
A survey of patients with anorexia nervosa found that vegetarians and vegans were over-represented and were more likely to have a persistent condition.
Compared to controls, individuals with an eating disorder history were significantly more likely to ever have been vegetarian (52% vs. 12%), to be currently vegetarian (24% vs. 6%), and to be primarily motivated by weight-related reasons (42% vs. 0%). The three recovery status groups (fully recovered, partially recovered, active eating disorder) did not differ significantly in percentiles endorsing a history of vegetarianism or weight-related reasons as primary, but they differed significantly in current vegetarianism (33% of active cases, 13% of partially recovered, 5% of fully recovered). Most perceived that their vegetarianism was related to their eating disorder (68%) and emerged after its onset.
The associations between meat avoidance and mood disorders in these studies are strong – they certainly dwarf any associations drawn between meat and any other diseases. We acknowledge this alone doesn’t demonstrate cause and effect. But it does suggest that there is a possibility of harm, and we must be cautious with population-wide advice.
New Zealand needs data on these correlations from within its own population before our public health experts start recommending meat avoidance to a population which has so many vulnerable members, in a country which is facing a mental health crisis.
Meat and cancer, Part 2 (Part 2).
The review goes lightly into the meat and colon cancer association, without a very clear discussion of the stats or the hopelessness of the “processed meat” definition. We’ve discussed this data before, but we’d like to share a much stronger and more convincing association – in 2006 people being treated for colon cancer, the insulin load and insulin index of the diet (a measure of the amount of insulin required to metabolise the food) was strongly correlated with cancer mortality.
The adjusted HRs for CRC-specific mortality comparing the highest to the lowest quintiles were 1.82 (95% CI: 1.20-2.75, Ptrend=0.006) for dietary insulin load and 1.66 (95% CI: 1.10-2.50, Ptrend=0.004) for dietary insulin index. We also observed an increased risk for overall mortality, with adjusted HRs of 1.33 (95% CI: 1.03-1.72, Ptrend=0.03) for dietary insulin load and 1.32 (95% CI: 1.02-1.71, Ptrend=0.02) for dietary insulin index, comparing extreme quintiles. The increase in CRC-specific mortality associated with higher dietary insulin scores was more apparent among patients with body mass index (BMI)⩾25 kg m-2 than BMI<25 kg m-2 (Pinteraction=0.01).
Now, while it’s true that protein requires insulin to be metabolised and that beef has a relatively high insulin load, it is also true that people eating low-carb diets get insulin levels very low whether they eat meat or not; such diets certainly reverse hyperinsulinaemia. Refined carbs are simply going to drive up the insulin effect of other foods like beef; you need protein and vitamins and minerals, and you don’t need sugar and artificial colourings.
It’s refined carbohydrate, sugar and starch, not protein or fat, which is most likley wasting the health of New Zealanders. We can demonstrate this by the improvements in health we see every day when people limit sugar and starch in their diets; not just biomarkers, but improvements in mood, pain, and exercise capacity. The health benefits of carbohydrate restriction are becoming more generally known and accepted with time.
The realisation that sugar and starch are fundamental to the nutrition-related harm that occurs in populations of developed countries is becoming mainstream now. The recent BMJ special issue “Food for Thought” is swimming in the science and policy of such a realisation.
There may even be environmental benefits; for one thing, you can now eat the fat from an animal instead of wasting it and replacing it with another food, for another thing, weight loss is a common side-effect of LCHF, even when used as a migraine cure.
And excess weight means people need to eat more. In 2012, biomass due to obesity was 3.5 million tonnes, the equivalent of 56 million people of average body mass (1.2% of human biomass globally). If the obesity epidemic could be entirely reversed, the food savings would be roughly equivalent to the annual food consumption of Australia and Canada combined (minus that of little New Zealand). This is perhaps a drop in the bucket globally, but it is still a lot of people.
Of course, we can treat and farm animals better and be more sustainable. That’s what the apex omnivore – us humans – must do if we want to leave even a half decent planet for the next generations.
 Godfray HCJ, Aveyard P, Garnett T et al. Meat consumption, health, and the environment. Science. 2018 Jul 20;361(6399). pii: eaam5324. doi: 10.1126/science.aam5324.
 Hibbeln JR, Northstone K, Evans J, Golding J. Vegetarian diets and depressive symptoms among men. J Affect Disord. 2018 Jan 1;225:13-17. doi: 10.1016/j.jad.2017.07.051. Epub 2017 Jul 28.
 Hibbeln JR, SanGiovanni JP, Golding J, et al. Meat Consumption During Pregnancy and Substance Misuse Among Adolescent Offspring: Stratification of TCN2 Genetic Variants. Alcoholism: Clinical & Experimental Research. Published online October 4 2017
 Bardone-Cone AM, Fitzsimmons-Craft EE, Harney MB, et al. The Inter-relationships between Vegetarianism and Eating Disorders among Females. Journal of the Academy of Nutrition and Dietetics. 2012;112(8):1247-1252. doi:10.1016/j.jand.2012.05.007.
 Yuan C, Bao Y, Sato K et al. Influence of dietary insulin scores on survival in colorectal cancer patients. Br J Cancer. 2017 Sep 26;117(7):1079-1087. doi: 10.1038/bjc.2017.272. Epub 2017 Aug 17.
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.
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 Portal and 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.
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.
Cardiovascular Disease Risk Assessment and Management for Primary Care.
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.
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, , , , Primary Prevention With Statin Therapy in the Elderly: New Meta-Analyses From the Contemporary JUPITER and HOPE-3 Randomized Trials.
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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