Friday, August 31, 2018

The Carb-Appropriate Podcast. Episode 4. feat. Pete Evans

The Carb-Appropriate Podcast show notes
Episode 4. Feat. Pete Evans, celebrity chef, paleo/keto guy, and health advocate

I met Pete originally when he was kind enough to promote the research and work that myself and my colleagues at AUT University were doing into lower-carb, real-food nutrition. Pete can certainly chat! So, strap in and enjoy! 😊

[Check out some of my work that Pete was nice enough to mention: ]

Pete talks about he went from being an award-winning chef from to a health advocate.

Primal Body Primal Mind provided much of the inspiration for Pete and his wife Nicola Robinson to start to change that way they cooked and ate at home and this lead Pete to realise the value of whole foods, lower-carb approach to eating.

4:50 – Pete talks about his transition from ‘Paleo’ (including creating paleo ‘substitute’ foods) into a more wholefoods-based paleo-keto diet

Overall, in this cast, Pete talked a lot about pro-inflammatory foods and cooking food from scratch

10:59 – “Be excited about the food that you create and the food you eat”
12:57 – “You can eat all the best food in the world and still suffer disease…or you could eat junk food and live to a ripe old age” [What else is going on other than just diet?]
19:00 – Is the next step in health care mind-body integrative work?

[A lot of general discussions ensue]

36:00 – Pete talks about some of the debate and backlash against his Paleo and Keto viewpoints [Hint: Follow the money? 😉 ]
50:00 – If you’re going to say that Paleo is ‘bad’ because it excludes food groups, shouldn’t the same criticism be levelled against a Vegan diet?  ¯\_(ツ)_/¯


If you’d like to check out more from Pete, go to:

Pete has a NEW range of collagen and bone broth super-blends available in New Zealand exclusively via

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Thursday, August 23, 2018

Is Coconut Oil Really POISON?!

Following the latest claims that Coconut Oil is ‘poison’ [] I thought it was a good chance to update the article below.

Rosemary Stanton, a well-known and respected nutritionist and researcher has suggested here 
[] that health claims surrounding Coconut Oil (CO) have been debunked. But have they really? And is CO a good addition to the diet…or is it a health-damaging fad?

Claim: “No study has found that coconut oil helps weight loss”
At least one study has shown a reduction in waist circumference. In a 12-week, randomised, double-blind clinical trial involving 40 women aged 20–40 years, participants were given a supplement of either 30 ml of coconut oil or soybean oil. Reductions in BMI were observed in both groups but only the group taking coconut oil reduced waist circumference.1 Waist circumference, as a proxy measure for abdominal adiposity, is a primary sign of insulin resistance and metabolic disorder.

What does that mean?
While more research is required, coconut oil might be better than vegetable oils for improving body-composition (and cardiovascular risk factors – more on that later!)

Claim: Coconut oil does not act like a medium-chain triglyceride
Health claims for coconut oil often rest on studies performed on MCTs. The claim made by Stanton and many others is that lauric acid (the C:12 fatty acid which makes up most of the coconut oil) does not act like an MCT and is digested in the same way as ‘normal’ dietary fats. In other words, like long-chain fatty acids (over 12 carbon chains in length) they will be bundled up with protein transporters and take up into the lymph and then deposited into the bloodstream as compared to MCTs which passively diffuse into the hepatic portal vein to be transported directly to the liver where cool stuff happens (like the creation of ketones!). While there IS limited of research demonstrating differences in the hepatic vs. lymphatic deposition of fatty acids of varying chain lengths it certainly appears that (with some exceptions) lymphatic deposition of fatty acids from triglycerides increases with carbon chain length.2 This has been demonstrated in rats by Mu and Hoy. In their study, recoveries from lymph of caprylic acid (8:0), capric acid (10:0), and lauric acid (12:0) were 7.3 +/- 0.9, 26.3 +/- 2.4, and 81.7 +/- 6.9%, respectively.3 That shows that little lauric acid is taken up into the liver for conversion to ketones But other research has shown conflicting results. For example, McDonald et al., have demonstrated that at low rates of infusion, 72% of lauric, 58% of myristic, 41% of palmitic, 28% of stearic, 58% of linoleic, and 68% of linolenic acid bypassed the lymphatic pathway.4 So, in that case, nearly ¾ of the lauric acid (12:0) was taken up by the liver. However as Bloom, and colleagues demonstrated as far back as 1951, deposition locations of lauric acid varies considerably between (animal) study subjects.5 and this is likely to be dependent on the position (sn-1, -2, or -3) of the fatty acid on the glycerol backbone and on individual factors of absorption. In our clinical research we have observed a direct effect of coconut oil on ketonaemia (the presence of ketones in the blood) and so we have a working hypothesis that in humans’ coconut oil, while not as ‘active’ as an MCT as the shorter chains (C:6-10) it does still exhibit similar activity. This is a hypothesis we will be testing in research commencing in 2018.

What does that mean?
While it isn’t transported to the liver in the same quantities as the ‘true’ MCTs and isn’t as ketogenic, lauric acid (from CO) is still ketogenic and offers some of the benefits of the C:6-10 fatty acids.

Claim: Coconut oil is ‘bad’ for the heart [Cliff’s paraphrasing!]
A common claim, due to it consisting predominantly of saturated fats, is that CO is detrimental to heart health. Thankfully most people have ditched the saturated fat-heart disease hypothesis…AND there is direct evidence which suggests that CO is not detrimental to cardiac health or other health outcomes.
In a comparison of Pacific peoples using differing amounts of CO, Prior and colleagues (1981) evaluated diets of atoll dwellers in Pukapuka and Tokelau in which coconut is the chief source of energy for both groups. Tokelauans exhibited higher saturated fat intake (63% of energy derived from coconut) than Pukapukans (34% energy derived from coconut) and had higher cholesterol levels. But despite this, cardiovascular diseases were uncommon in both groups, with no evidence that higher saturated fat intake, and higher coconut intake providing a harmful effect 6.
I have spoken in the past to my good friend and colleague (and advisor to the Holistic Performance Institute) Dr Sridhar Maddela about the extensive use of coconut oil as a traditional cooking oil in the Southern Indian province of Kerala. In this province, the traditional and common use of CO has been (falsely) implicated as a reason for high Coronary Heart Disease (CHD) rates. However, a study comparing 16 age and sex-matched controls performed in Kerala to explore this presumed link between coconut oil and heart disease risk found that CO consumption was similar in both groups (with and without CHD).7 The groups did not differ in fat, saturated fat or cholesterol consumption, implying no specific role for coconut oil or coconut consumption in this population for CHD risk. It has been further noted (in this population) that the lipid composition of arterial plaques is not altered by replacing coconut oil with sunflower oil.8 Indeed, there has been an alarming rise in the prevalence of CHD and Type-2 Diabetes in India attributed in part to the replacement of traditional cooking fats with refined vegetable oils—resulting in calls to switch ‘back’ to a combination of different types of fats including the traditional cooking fats like ghee, coconut oil and mustard oil to reduce the risk of CHD and diabetes.9
A community based longitudinal study in Cebu, Philippines found a positive, albeit small correlation between CO and HDL cholesterol, with no worsening of HDL-Total Cholesterol ratio or triglycerides.10
In the study comparing soybean to coconut oil, the coconut oil treated group exhibited higher levels of ‘good cholesterol’ and lower levels of ‘bad cholesterol’. The soybean oil treated group demonstrated reduced HDL (‘good cholesterol’), increased cholesterol and (‘bad’) LDL cholesterol. This result suggests that coconut oil does not cause dyslipidaemia.1
A report by the Food and Agriculture Organisation of the United Nations has stated: “All available population studies show that dietary coconut oil does not lead to high serum cholesterol nor to high coronary heart disease mortality or morbidity rate.”11

Update: In recent studies, the heart-healthy properties of CO have been further demonstrated.
In a study of 96 men and women between 50 and 75 years or age, there was no difference between VCO and olive oil for changes in LDL-c, but VCO significantly increased HDL-c compared to either butter or olive oil. There were no significant differences in changes in weight, BMI, blood glucose, adiposity, or blood pressure between the butter, VCO, and olive oil groups.12
In another recent study, 15 women randomised to receive either VCO or olive oil as control showed no difference in insulin homeostasis, LDL-c, HDL-c, uric acid, or triglycerides.13

What does that mean?
Coconut oil is fine. Don’t stress…it’s not bad for your heart!

Claim: Coconut oil is not anti-microbial
Stanton is correct that the anti-microbial effects of monolaurin (a breakdown product of lauric acid) cannot necessarily be translated to humans or that the body can make monolaurin from lauric acid in vivo (in the body) and while it’s always important to interpret any emerging evidence with a degree of caution, there is preliminary evidence for the use of coconut oil itself as an antimicrobial. Virgin coconut oil in its whole form doesn’t typically exert anti-bacterial actions and must be broken down to its monoglyceride or free fatty-acid forms to exert these effects.14, 15 Virgin coconut oil does not impede growth of Clostridium dificile but lipolyzed coconut oil does and lauric acid has greater antimicrobial effect than either capric (C:10) or caprylic (C:8) fatty acids.16 However, when used as a moisturizer coconut oil resulted in 19 of 20 people who had tested positive for Staphylococcus aureus colonies being retested as negative after 4 weeks.
Coconut oil may have greater application to fungal infections. A 2007 paper, Ogbolu and colleagues suggested “Coconut oil should be used in the treatment of fungal infections in view of emerging drug-resistant Candida species”17
In a pilot study of 60 adolescents with gingivitis (gum disease) and plaque, oil pulling with coconut oil resulted in a significant reduction in both plaque and gingivitis over 30 days.18
Topical application of coconut oil increases the speed of skin wound healing in rats.19 Animal studies also suggest analgesic (pain reducing) and anti-inflammatory effects of coconut oil.20 High doses (10ml/kg) of CO have demonstrated a hepatoprotective (liver protecting) effect against paracetamol-induced liver damage in rats.21
Update: A study of 72 preterm infants compared standard-care vs topical coconut oil. Pre-term infants have ‘fragile’ skin that is vulnerable and provides an inadequate protective barrier. Topical coconut oil maintained a better skin condition than standard-care, without adverse effects.22

What does that mean?
I’m not going to hang my hat on CO being an antimicrobial wonder drug BUT based on the evidence to date it does seem to exhibit some beneficial effects on impeding some pathogens and aiding wound healing.

As for tooth whitening?...
I don’t know and to be honest I don’t care. People get hung up too much on criticizing certain foods because it doesn’t fit their worldview.

When in doubt go back to the research…and in this case, the weight of evidence shows us that coconut oil, while not being the cure-all that some claim, is a healthy addition to the diet and may offer some interesting functional benefits.

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1.            Assunção M, Ferreira H, dos Santos A, Cabral C, Jr., FlorĂȘncio TMT. Effects of Dietary Coconut Oil on the Biochemical and Anthropometric Profiles of Women Presenting Abdominal Obesity. Lipids. 2009;44(7):593-601.
2.            Thomson ABR, Keelan M, Garg ML, Clandinin MT. Intestinal aspects of lipid absorption: in review. Canadian Journal of Physiology and Pharmacology. 1989;67(3):179-91.
3.            Mu H, Hoy CE. Effects of different medium-chain fatty acids on intestinal absorption of structured triacylglycerols. Lipids. 2000;35(1):83-9.
4.            McDonald GB, Saunders DR, Weidman M, Fisher L. Portal venous transport of long-chain fatty acids absorbed from rat intestine. American Journal of Physiology - Gastrointestinal and Liver Physiology. 1980;239(3):G141-G50.
5.            Bloom B, Chaikoff IL, Reinhardt WO. Intestinal lymph as pathway for transport of absorbed fatty acids of different chain lengths. American Journal of Physiology--Legacy Content. 1951;166(2):451-5.
6.            Prior IA, Davidson F, Salmond CE, Czochanska Z. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. The American Journal of Clinical Nutrition. 1981;34(8):1552-61.
7.            Kumar PD. The Role of Coconut and Coconut Oil in Coronary Heart Disease in Kerala, South India. Tropical Doctor. 1997;27(4):215-7.
8.            Palazhy S, Kamath P, Rajesh PC, Vaidyanathan K, Nair SK, Vasudevan DM. Composition of Plasma and Atheromatous Plaque among Coronary Artery Disease Subjects Consuming Coconut Oil or Sunflower Oil as the Cooking Medium. Journal of the American College of Nutrition. 2012;31(6):392-6.
9.            Sircar S, Kansra U. Choice of cooking oils--myths and realities. J Indian Med Assoc. 1998;96(10):304-7.
10.         Feranil AB, Duazo PL, Kuzawa CW, Adair LS. Coconut oil is associated with a beneficial lipid profile in pre-menopausal women in the Philippines. Asia Pacific journal of clinical nutrition. 2011;20(2):190-5.
11.         Kaunitz H, Dayrit, C.S. . Coconut Oil Consumption and Coronary Heart Disease: Food and Agriculture Organisation of the United Nations; N.D [
12.         Khaw K-T, Sharp SJ, Finikarides L, Afzal I, Lentjes M, Luben R, et al. Randomised trial of coconut oil, olive oil or butter on blood lipids and other cardiovascular risk factors in healthy men and women. BMJ open. 2018;8(3).
13.         Valente FX, CĂąndido FG, Lopes LL, Dias DM, Carvalho SDL, Pereira PF, et al. Effects of coconut oil consumption on energy metabolism, cardiometabolic risk markers, and appetitive responses in women with excess body fat. Eur J Nutr. 2018;57(4):1627-37.
14.         Sia C, Yim H, Lai C. Commercial virgin coconut oil: assessment of antimicrobial potential. Asian Journal of Food and Agro-Industry. 2010;3(6):567-79.
15.         Tangwatcharin P, Khopaibool P. Activity of virgin coconut oil, lauric acid or monolaurin in combination with lactic acid against Staphylococcus aureus. The Southeast Asian journal of tropical medicine and public health. 2012;43(4):969-85.
16.         Shilling M, Matt L, Rubin E, Visitacion MP, Haller NA, Grey SF, et al. Antimicrobial Effects of Virgin Coconut Oil and Its Medium-Chain Fatty Acids on Clostridium difficile. Journal of medicinal food. 2013;16(12):1079-85.
17.         Ogbolu DO, Oni AA, Daini OA, Oloko AP. In Vitro Antimicrobial Properties of Coconut Oil on Candida Species in Ibadan, Nigeria. Journal of medicinal food. 2007;10(2):384-7.
18.         Peedikayil FC, Sreenivasan P, Narayanan A. Effect of coconut oil in plaque related gingivitis — A preliminary report. Nigerian Medical Journal : Journal of the Nigeria Medical Association. 2015;56(2):143-7.
19.         Nevin KG, Rajamohan T. Effect of Topical Application of Virgin Coconut Oil on Skin Components and Antioxidant Status during Dermal Wound Healing in Young Rats. Skin Pharmacology and Physiology. 2010;23(6):290-7.
20.         Intahphuak S, Khonsung P, Panthong A. Anti-inflammatory, analgesic, and antipyretic activities of virgin coconut oil. Pharmaceutical Biology. 2010;48(2):151-7.
21.         Zakaria ZA, Rofiee MS, Somchit MN, Zuraini A, Sulaiman MR, Teh LK, et al. Hepatoprotective Activity of Dried- and Fermented-Processed Virgin Coconut Oil. Evidence-Based Complementary and Alternative Medicine. 2011;2011:8.
22.         Strunk T, Pupala S, Hibbert J, Doherty D, Patole S. Topical Coconut Oil in Very Preterm Infants: An Open-Label Randomised Controlled Trial. Neonatology. 2018;113(2):146-51.

Tuesday, August 21, 2018

Response to Consumer Magazine Claims about Nuzest Clean Lean Protein

In a recent Consumer Magazine article on protein supplements, several claims were made about products I co-developed as one of the founders and formulators for Nuzest. While I think on balance Consumer do an excellent job, in this case, the claims about Clean Lean Protein and Just Fruit and Veg were spurious.

Is Clean Lean Protein high in salt?

According to consumer magazine Clean Lean Protein is high in salt.
Nuzest Clean Lean Protein Vanilla (1428mg)”

It is disingenuous to suggest that this is a ‘high’ salt load. A serve of CLP is 25 g, which would provide 357 mg of sodium. To put this in context, mortality and morbidity are increased at both high and low levels of sodium intake. (1, 2) In other words, there is a ‘U-shaped curve’ of morbidity (disease) related to extremes of intake, whether high or low. The range within which no discernible health effects are seen lies between 2,645 and 4,945 mg (1) or as high as 6000mg. (2) So, CLP provides only 6-13% of the safe daily value of sodium. As protein powders are designed to be used as major components of meals, this is a trivial amount of sodium.

Saturated Fat content of Just Fruit and Veg

“Nuzest Just Fruit and Vege Fresh Coconut topped the protein powder chart for saturated fats with 8g.”

Again, this is a trivial amount. In one serving of Just Fruit and Veg there is 3 g of fat, of which 2 g is saturated (a mere 18 calories). This amount is unlikely to cause any substantive effect in the body. Dose notwithstanding, we would question the caution against saturated fat.
Almost all systematic reviews and meta-analyses find little to no association between saturated fat intake and mortality. (3-5)  A ‘gold-standard’ Cochrane database review of randomised studies on the effect of modified or reduced fat interventions on total and cardiovascular disease (CVD) by Hooper and colleagues, there was no overall effect of reduced saturated fat diets on either total mortality (relative risk 0.98, 95% CI: 0.93 to 1.04) or for CVD mortality (relative risk: 0.94, 95% CI 0.85 to 1.04). (6) 
While substitution studies do show that replacement of some saturated fat with polyunsaturated fats improves CVD mortality outcomes, (7)  they do not find that replacing saturated fat with monounsaturated fat or carbohydrate similarly improves outcomes. So, it should be concluded that polyunsaturated fats (i.e. essential fats) are important and not that saturated fats are bad. If saturated fat independently worsened outcomes, any reduction by replacement with nutrients deemed ‘heart healthy’ (carbohydrates and monounsaturated fats) should improve outcomes, which it doesn’t. In a meta-analysis of fatty acid substitution RCTs Mozaffarian et al., stated that we “cannot distinguish between potentially distinct benefits of increasing polyunsaturated fatty acids (PUFA) versus decreasing saturated fatty acids (SFA).(8)  Therefore, based on the weight of evidence, saturated fats in the context of an otherwise healthy diet don’t increase your risk of either cardiac disease, mortality, or all-cause mortality.

Can you get all you need from diet?

 “You can get all the vitamins and minerals you need from a well-balanced diet. When you consume more than what you need in multivitamins and supplemented products, some are excreted in your urine, so it’s just a waste of money,”

While of course food comes first, and you can get all you require from diet, the reality is that most people do not.
US Department of Agriculture data shows that some fresh produce (vegetables, fruits berries) may only provide around half the amounts of some vitamins and minerals that they did in the 1950s. (9)  So, while we have been eating more (and getting bigger!) over time, and taking in more than enough calories and ‘fuel’, we aren’t necessarily getting enough of the ‘little guys’, the vitamins, minerals and secondary nutrients that act as co-factors for energy creation, hormone and neurotransmitter creation and that help to reduce the oxidative damage resulting from both environmental and lifestyle stressors, and that we create as part of our normal process of energy created within the cell.
Estimates from the New Zealand Ministry of Health ‘NZ Adult Nutrition Survey’ of 2008/2009 suggest that many New Zealanders are not getting the recommended amounts of many of the vitamins and minerals from their diets. (10)
Some of the key findings included:
·        Around 20% of people fail to get enough vitamins A (one of our major anti-oxidant vitamins, vital for gene expression, eye health and cell division), B1 and B6 (both essential for energy creation)
·        8% of people fail to get enough B12. B12 is required for proper functioning of nerve cells and without adequate B12 people can suffer from a form of anaemia and ultimately lack of B12 can permanently damage neurons.
·        Nearly 10% of women don’t get enough iron. Iron deficiency results in anaemia, lethargy and loss of muscle strength and endurance.
·        Around 25% of people don’t consume enough zinc. Zinc is extremely important for immune function and for the creation of testosterone. Interestingly nearly 40% of males may not get adequate zinc from their diet, which could increase the risk of colds, flu and reduce the ability to build muscle.
·        45% of people don’t get enough Selenium, a mineral lacking in New Zealand soils that is vital to thyroid function and metabolic rate.

Multinutrient formulas improve mortality outcomes for cancer and stroke and provide an overall protective benefit for cancer and heart disease, along with improvements in all-cause mortality. (11, 12) They can also reduce perceived stress, (13) improve sleep, (14) improve memory and cognition. (15) Overall, multis are a safe and effective way to ensure a healthy intake of essential and beneficial nutrients. (16)

Protein needs are underestimated

“While it’s true you need protein for building and repairing tissue and muscles, Ms Carey said you can get all you need from a balanced diet.
Your daily protein requirement can be calculated as roughly 0.8 to 1g per kilo of body weight. So, if you’re 70kg, you need between 56 and 70g of protein.
The latest New Zealand Adult Nutrition Survey found 98% of adults got their required daily protein intake, with some getting more than double what they needed.
Research shows that even high-performance athletes with strenuous workout regimes get no added benefit from any more than 2g of protein per kg of body weight.”

Many people, in contrast to the statements above, do not get enough protein to thrive.
In both NZ and the US, the average intake of protein is around 100 g and 70 g for males and females respectively. (10, 17) While this is higher than the recommended daily intake of 0.8 g/kg/day it is below the recommended levels for both performance, and for offsetting age-related muscle loss. Analysis of US eating patterns has suggested that people should actually be aware of eating enough protein, not reducing their protein intake, especially as protein intakes decline as we age. (18)
Protein is important for everyone and especially important as we age. Age-related muscle loss is common and is a contributing factor to falls and bone and joint injury. This muscle loss also increases our risk of metabolic disorders like diabetes. In older adults, high-protein nutritional supplements are associated with lower hospital admissions and fewer health complications. (19) Increased protein also allows us to retain more lean mass and lose more fat. (20)(21) Higher protein diets are also good for ‘cardiometabolic’ health. Increased dietary protein has a beneficial effect on blood pressure, triglycerides (one of the most important markers of poor cardiovascular and metabolic health), and reduces body fat. (22, 23) For those dieting, or even those who are just habitual under-eaters, an increased protein intake of up to 2.5g per kilogram of body weight is likely to help offset muscle loss, and thus improve body composition (muscle to fat ratio). (24) This level of protein is around 3 x higher than the recommended daily allowance of 0.8g per kg body weight. Not only that but for ‘weekend warriors’ training for sports, or at the gym, protein taken after training might reduce soreness. (25) And in healthy adults, over the long term, protein is likely to increase lean muscle and help to improve strength and power. (26)

Are animal-derived proteins superior?

"Choosing whey-, egg- or soy-based protein powders is also better because they have good amino acid profiles and are quickly digested.
Protein found in meat, fish, poultry and dairy products has all 20 of the amino acids our bodies need. Two plant foods, soy and quinoa, are also complete proteins. Other foods, such as peas, tofu and oats, also have protein, but not all of the amino acids. So, while you’ll still get protein from a pea-based powder, it’s not a complete option."

Pea protein isolate, like that in Clean Lean Protein has an amino acid profile that compares favourably with the recommended amino acid pattern proposed by the Institute of Medicine of the United States National Institutes of Health. (27) It contains all 9 essential amino acids and in an evaluation of pea protein isolate vs. whey protein both protein-types elicited nearly identical increases in muscle thickness when compared with placebo. (28)
Also worth considering, while dairy is fine for most people, it is also a common allergen, and there appears to be a rising incidence of milk protein intolerance and allergy. (29) Egg too can be a common allergen, and soy is high in phytic acid and other ‘anti-nutrients’ making it less favourable than pea protein isolate.

1.            Graudal N, JĂŒrgens G, Baslund B, Alderman MH. Compared With Usual Sodium Intake, Low- and Excessive-Sodium Diets Are Associated With Increased Mortality: A Meta-Analysis. American Journal of Hypertension. 2014.
2.            Alderman MH, Cohen HW. Dietary Sodium Intake and Cardiovascular Mortality: Controversy Resolved? American Journal of Hypertension. 2012;25(7):727-34.
3.            Skeaff CM, Miller J. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab. 2009;55(1-3):173-201.
4.            Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American journal of clinical nutrition. 2010;91(3):535-46.
5.            Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med. 2009;169(7):659-69.
6.            Hooper L, Summerbell CD, Thompson R, Sills D, Roberts FG, Moore H, et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst Rev. 2011(7):CD002137.
7.            Jakobsen MU, O'Reilly EJ, Heitmann BL, Pereira MA, Balter K, Fraser GE, et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009;89(5):1425-32.
8.            Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010;7(3):e1000252.
9.            Davis DR, Epp MD, Riordan HD. Changes in USDA Food Composition Data for 43 Garden Crops, 1950 to 1999. Journal of the American College of Nutrition. 2004;23(6):669-82.
10.         University of Otago and Ministry of Health. A Focus on Nutrition: Key findings of the 2008/09 New Zealand Adult Nutrition Survey. Wellington; 2011.
11.         Huang H-Y, Caballero B, Chang S, Alberg AJ, Semba RD, Schneyer CR, et al. The Efficacy and Safety of Multivitamin and Mineral Supplement Use To Prevent Cancer and Chronic Disease in Adults: A Systematic Review for a National Institutes of Health State-of-the-Science Conference. Annals of Internal Medicine. 2006;145(5):372-85.
12.         Alexander DD, Weed DL, Chang ET, Miller PE, Mohamed MA, Elkayam L. A Systematic Review of Multivitamin–Multimineral Use and Cardiovascular Disease and Cancer Incidence and Total Mortality. Journal of the American College of Nutrition. 2013;32(5):339-54.
13.         Macpherson H, Rowsell R, Cox KHM, Scholey A, Pipingas A. Acute mood but not cognitive improvements following administration of a single multivitamin and mineral supplement in healthy women aged 50 and above: a randomised controlled trial. AGE. 2015;37(3):1-10.
14.         Sarris J, Cox KHM, Camfield DA, Scholey A, Stough C, Fogg E, et al. Participant experiences from chronic administration of a multivitamin versus placebo on subjective health and wellbeing: a double-blind qualitative analysis of a randomised controlled trial. Nutrition Journal. 2012;11(1):1-10.
15.         Harris E, Macpherson H, Vitetta L, Kirk J, Sali A, Pipingas A. Effects of a multivitamin, mineral and herbal supplement on cognition and blood biomarkers in older men: a randomised, placebo-controlled trial. Human Psychopharmacology: Clinical and Experimental. 2012;27(4):370-7.
16.         Biesalski HK, Tinz J. Multivitamin/mineral supplements: rationale and safety – A systematic review. Nutrition.
17.         Moshfegh A, Goldman J, Cleveland L. What we eat in America, NHANES 2001-2002: usual nutrient intakes from food compared to dietary reference intakes. US Department of Agriculture, Agricultural Research Service. 2005;9.
18.         Fulgoni VL. Current protein intake in America: analysis of the National Health and Nutrition Examination Survey, 2003–2004. The American Journal of Clinical Nutrition. 2008;87(5):1554S-7S.
19.         Cawood AL, Elia M, Stratton RJ. Systematic review and meta-analysis of the effects of high protein oral nutritional supplements. Ageing Research Reviews. 2012;11(2):278-96.
20.         Kim JE, O’Connor LE, Sands LP, Slebodnik MB, Campbell WW. Effects of dietary protein intake on body composition changes after weight loss in older adults: a systematic review and meta-analysis. Nutrition reviews. 2016;74(3):210-24.
21.         Kim JE, Sands L, Slebodnik M, O’Connor L, Campbell W. Effects of high-protein weight loss diets on fat-free mass changes in older adults: a systematic review (371.5). The FASEB Journal. 2014;28(1 Supplement).
22.         Altorf – van der Kuil W, Engberink MF, Brink EJ, van Baak MA, Bakker SJL, Navis G, et al. Dietary Protein and Blood Pressure: A Systematic Review. PloS one. 2010;5(8):e12102.
23.         Santesso N, Akl EA, Bianchi M, Mente A, Mustafa R, Heels-Ansdell D, et al. Effects of higher- versus lower-protein diets on health outcomes: a systematic review and meta-analysis. Eur J Clin Nutr. 2012;66(7):780-8.
24.         Helms ER, Zinn C, Rowlands DS, Brown SR. A Systematic Review of Dietary Protein during Caloric Restriction in Resistance Trained Lean Athletes: A Case for Higher Intakes. International Journal of Sport Nutrition and Exercise Metabolism. 2014;24(2):127-38.
25.         Pasiakos SM, Lieberman HR, McLellan TM. Effects of Protein Supplements on Muscle Damage, Soreness and Recovery of Muscle Function and Physical Performance: A Systematic Review. Sports Medicine. 2014;44(5):655-70.
26.         Pasiakos SM, McLellan TM, Lieberman HR. The Effects of Protein Supplements on Muscle Mass, Strength, and Aerobic and Anaerobic Power in Healthy Adults: A Systematic Review. Sports Medicine. 2015;45(1):111-31.
27.         Hansen K, Shriver T, Schoeller D. The effects of exercise on the storage and oxidation of dietary fat. Sports Med. 2005;35.
28.         Babault N, PaĂŻzis C, Deley G, GuĂ©rin-Deremaux L, Saniez M-H, Lefranc-Millot C, et al. Pea proteins oral supplementation promotes muscle thickness gains during resistance training: a double-blind, randomized, Placebo-controlled clinical trial vs. Whey protein. Journal of the International Society of Sports Nutrition. 2015;12(1):3.

29.         Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al. The prevalence of food allergy: A meta-analysis. Journal of Allergy and Clinical Immunology. 2007;120(3):638-46.

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