- That whole plants and animals are likely to be good for you and your chronic disease risk
- That foods which reduce inflammation are good for reducing chronic disease
- That sugar and processed carbs are not good, especially if you are insulin resistant (most of the vulnerable populations)
- That hyperinsulinaemia and chronic inflammation (both highly inter-related and can cause one another) are a problem and part of the mechanism for developing CVD and other chronic diseases.
- The Standard American industrial food diet and lifestyle is toxic, and much of the research showing different ways of eating show benefits simply because this diet is so bad.
- Trans fats and high omega 6 seed oils are inflammatory
- The interplay between hormonal physiology, built environment, food, and physical activity is complex. This influences catabolic and anabolic states and therefore human energy homeostasis. We don’t know exactly how the system works. We have made the mistake (using Einstein’s words “make it as simple as possible but no simpler”) to describe the calories in and calories out dogma which we need to move on from.
- That SFA from whole healthy animals has any proven negative effect on human health in the context of the above (whole food eating).
- Attributing changes in populations to specific nutrients in a complex multifactorial disease using epidemiology which measures eating is fraught and is giving answers the opposite to those observed in decent robust RCTs.
- That low carb high fats diets are safe, efficacious, and useful for the public.
My response to the technical points in the media release asking for evidence today
- The actual trials showing SFA reduction and health improvements are fraught because they are still mainly in the Standard American Diet (SAD) paradigm with small dietary modifications. I agree that SFA intake in the context of the SAD might be problematic. What I still have a problem with, in these trials, is that many (most) still use a control group eating the same old food. Putting anyone on a diet different from the SAD will probably help. Here’s the latest meta analysis. In fact, the reality is that consuming SFA has positive effects on HDL cholesterol and reduces triglycerides.
- I’m not bothering with an in-depth rebuttal of the population studies. There’s just too much (uncontrolled and unmeasured) going on there, with poor food measurement to say saturated fat causes anything.
- I particularly draw to your attention to the bit in the media release directed straight at me (just say my name guys I am comfortable with that). “However, the group suggests that those who advocate for radical new dietary approaches have a responsibility to provide convincing peer-reviewed evidence of long term benefit as well as absence of harm. Such evidence does not exist for diets high in saturated and total fat, and very low in carbohydrate”. I have tried to address these issues in depth below. But first, how a diet full of whole plants and animals, similar to what humans have eaten the whole time they have been on the planet (up until recently, when human life expectancy halved (agricultural revolution) and then got full of disability from chronic disease (last few decades)) is radical is beyond my reasoning. Read the latest nutritional biochemistry and draw your own conclusions.
- Low carbohydrate diets being safe, efficacious and useful? RCT and mechanistic evidence shows that dietary saturated fat alone, in the context of a low carb diet doesn’t have the proposed cardio-metabolic risk effects of being harmful. In fact, things all go the other way (improve) which is a very good sign. I have put some references below, but also here’s a recent meta analysis of the clinical trials of low carb high fat diets and their metabolic effects. People generally do better metabolically, adhere better, and control blood glucose and insulin better on low carb high fat diets than other diets. Much of the reason for this (expanded below) is that when you become insulin resistant then a lower fat diet will provoke high insulin which only adds to the problem. Here is an excellent summary of the 23 RCTs on low carb high fat
- More on long term safety – Jim Mann’s main point on the stuff.co.nz article and media release about low carb high fat was around long term efficacy and safety. He does have a point – you can study this through RCTs, but the long term epidemiology isn’t there for eating actual whole plants and animals (short of the work on healthy indigenous populations, and that this is the sort of diet humans have eaten for 99.9% of the time they have been on the planet). There is certainly no evidence of harm – some people like to quote the Swedish women’s study to show there is harm of a high fat, high protein diet. I am not promoting this combination of eating. The epidemiology in this study is woeful because the lowest decile of population carb eaters was still getting 40 percent of their calories from carbs who also had to be in the highest decile of protein eaters – again not what I suggest – had poorer health outcomes. Again if the cardio- metabolic risk factors are worth anything – then people do better. Here’s a good dissection of this Swedish paper.
I think this shows how epidemiology sometimes gives us what we want to see. I agree that more work needs to be done. My starting hypothesis is to look at human nutrition through an evolutionary biology lens – what food environments are humans adapted to? And what is the physiology around this? I think we have to understand how and why insulin resistance happens and how that relates to chronic disease through inflammatory processes. I particularly recommend to you this paper which has a brilliant and comprehensive take on the evolutionary nutritional biochemistry and chronic disease development. BTW – the 40% CHO diet and high protein combination in the Swedish study showing the highest CVD is very much the type of mix Professor Mann has advocated (to me at least) he would support.
- Some longer-term data on Type 1 diabetics and low carb high fat diets – good efficacy and safety.
- Mechanistically high SFA doesn’t translate to high plasma SFA in the context of low carb diets – see reference.
- I agree that people respond differently to different diets. Insulin resistance is important as to what diet we can tolerate. Hyperinsulinaemia induces the direct and indirect effects for the major chronic diseases. Impaired glucose tolerance doesn’t catch this until end stage. Many many people get glucose into their cells at the right rate, but with hyperinsulinaemia. Complex carbs may not help, and in fact be even worse because the carbs are digested slowly provoking longer hyperinsulinaemia – a reference. We will publish our analysis of this soon. But in the meantime see the work of Dr Joseph Kraft.
- The only way to diagnose this is a dynamic glucose tolerance test measuring insulin. We have a database of 15,000 of these with insulin for up to five hours post OGTT. You will see the pattern of hyperinsulinaemia with normal glucose tolerance decades before impaired glucose tolerance.
- I contend that virtually every CVD risk factor either causes insulin resistance through inflammatory or other processes e.g. Sleep, stress, sugar, alcohol, smoking, pollution and so on. Obviously some have other effects too (e.g. smoking). But also that age and ethnicity affect Insulin sensitivity – Maori and Pacific are likely to be more prone to the above.
- Here’s the kicker for me – in terms of health inequalities the current dietary guidelines probably perpetuate health inequities because the least at risk do the best and stay healthy. So even if the two types of dietary guidance are efficacious – which they are – albeit not equally distributed in their efficacy AND there seems to be no evidence of harm from a lower carb high fat – then we have no option but to go the high fat route because of the inequalities – although I acknowledge we need more work to understand this. That’s the reason I am pursuing this.
Extra references to 23 RCTs showing good outcomes for low carb diets compared to other diets. Actual data summarised here very nicely too
1. Foster GD, et al. A randomized trial of a low-carbohydrate diet for obesity. New England Journal of Medicine, 2003.
2. Samaha FF, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. New England Journal of Medicine, 2003.
3. Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. The Journal of Pediatrics, 2003.
4. Brehm BJ, et al. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. The Journal of Clinical Endocrinology & Metabolism, 2003.
5. Aude YW, et al. The national cholesterol education program diet vs a diet lower in carbohydrates and higher in protein and monounsaturated fat. Archives of Internal Medicine, 2004.
6. Yancy WS Jr, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia. Annals of Internal Medicine, 2004.
7. JS Volek, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutrition & Metabolism (London), 2004.
8. Meckling KA, et al. Comparison of a low-fat diet to a low-carbohydrate diet on weight loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. The Journal of Clinical Endocrinology & Metabolism, 2004.
9. Nickols-Richardson SM, et al. Perceived hunger is lower and weight loss is greater in overweight premenopausal women consuming a low-carbohydrate/high-protein vs high-carbohydrate/low-fat diet. Journal of the American Dietetic Association, 2005.
10. Daly ME, et al. Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes. Diabetic Medicine, 2006.
11. McClernon FJ, et al. The effects of a low-carbohydrate ketogenic diet and a low-fat diet on mood, hunger, and other self-reported symptoms. Obesity (Silver Spring), 2007.
12. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study. The Journal of The American Medical Association, 2007.
13. Halyburton AK, et al. Low- and high-carbohydrate weight-loss diets have similar effects on mood but not cognitive performance. American Journal of Clinical Nutrition, 2007.
14. Dyson PA, et al. A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects. Diabetic Medicine, 2007.
16. Shai I, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. New England Journal of Medicine, 2008.
17. Keogh JB, et al. Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity. American Journal of Clinical Nutrition, 2008.
18. Tay J, et al. Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. Journal of The American College of Cardiology, 2008.
19. Volek JS, et al. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids, 2009.
20. Brinkworth GD, et al. Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 months. American Journal of Clinical Nutrition, 2009.
21. Hernandez, et al. Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet. American Journal of Clinical Nutrition, 2010.
22. Krebs NF, et al. Efficacy and safety of a high protein, low carbohydrate diet for weight loss in severely obese adolescents. Journal of Pediatrics, 2010.
23. Guldbrand, et al. In type 2 diabetes, randomization to advice to follow a low-carbohydrate diet transiently improves glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss. Diabetologia, 2012.