The New Zealand Heart Foundation state that the “Tick Programme helps New Zealanders make healthier food choices” but evidence would suggest that many of the foods that sport the Heart Foundation’s Tick are exactly the type of foods that do not support making of better health.
The guidelines still fail to adequately address glycaemic loads from non-sugar choices and for example, provide a highly favourable weighting to wholegrain foods including breads and other high carbohydrate, highly glycaemic and highly insulinergic foods, along with a continued preference for low-fat dairy despite there being no compelling evidence that low-fat dairy offers any benefit. In fact it has been demonstrated that (contrary to the authors hypothesis) lower fat varieties of milk products are associated with weight gain but full-fat dairy is not (Berkey, Rockett, Willett, & Colditz, 2005), and amongst other evidence a recent review has concluded that recommendations to reduce dairy fat are in contrast to the available evidence (Kratz, Baars, & Guyenet, 2013).
Many of the guidelines (including for example that of low-fat dairy preference) are based on the a priori position that energy intake trumps other factors related to diet. At HPN we contend that this is not in fact the case. There are efficiencies and inefficiencies within any living system and thus a calorific argument based solely on laboratory calorimetry fails to take these into account. Feinman and Fein (2004) have noted that “’a calorie is a calorie’ violates the second law of thermodynamics” due to its relative inability to account for metabolic advantages (such as alterations in lipogenesis, lipolysis, protein accretion and catabolism) arising from various dietary strategies incorporating differing macronutrient contents.
A reason for continuing to endorse a low-fat high-carbohydrate diet is based on the greater energy density of fats compared to carbohydrates. The Atwater factor for carbohydrate is 4 calories per gram compared to 9 calories per gram for fats. Thus avoiding fat equates to fewer calories per mouthful and therefore a greater likelihood of weight gain. Willet and Liebel (2002) concluded that "within the United States, a substantial decline in the percentage of energy from fat during the last two decades has corresponded with a massive increase in the prevalence of obesity. Diets high in fat do not appear to be the primary cause of the high prevalence of excess body fat in our society, and reductions in fat will not be a solution (p.1)."
The failure of high-carbohydrate and low-fat diet recommendations is indicated by the consistent lowering of carbohydrate recommendations over the last 20 years. The World Health Organisation (WHO) published dietary guidelines in 1998 (World Health Organisation, 1998) suggesting a range of 55%-70% of calories come from carbohydrate, but a 2007 update suggests that there is little actual evidence for the lower threshold and suggesting this could be lowered to 50% of calories (Mann et al., 2007). Indeed Nutrient Reference Values (NRV) for New Zealand and Australia state that the diet should contain a only a minimum of 45% of its calories from carbohydrate (Dietitians Association of Australia, 2013).
In contrast to the recommendations favouring a high carbohydrate (and consequently low fat and low-moderate protein) high-protein, low-carbohydrate (HPLC) diets appear to enhance weight-loss and improve glycaemic control, with a greater loss of body-fat and reduced loss of lean body mass compared to high-carbohydrate diets. This is due to a number of factors that are yet to be fully elucidated including (but perhaps not limited to): increased satiety, increased thermogenesis, muscle sparing and enhanced glycaemic control (Farnsworth et al., 2003; Labayen, Diez, Gonzalez, Parra, & Martinez, 2002; Layman & Baum, 2004; Piatti et al., 1994).
Noakes and others have demonstrated that there may be further nutritional benefits (aside from weight-loss which was demonstrated) resulting from higher protein diets—with greater fat loss in the obese exhibiting high triacylglycerol TAG)counts, reduced TAG and improved B12 status compared to higher carbohydrate diets (Noakes, Keogh, Foster, & Clifton, 2005).
The positive effects of higher protein intake on anthropometry in particular can be explained due to several factors, including increased satiety and thermogenesis when compared to equivalent amounts of either carbohydrates or fat (Keller, 2011). There is also higher thermic effect of feeding (TEF) associated with protein ingestion as compared to either carbohydrate or fat (Johnston, Day, & Swan, 2002; Robinson et al., 1990; Westerterp, 2004) A higher protein intake is considered to be more satiating than the carbohydrate it is displacing. A 2004 review by Halton and Hu (2004) found there to be convincing evidence that a higher protein intake increases thermogenesis and satiety compared to diets of a lower protein content.
Low carbohydrate, high fat diets (often with low-to-moderate protein) likewise have demonstrated sufficient evidence to be considered a therapeutic option for the primary and adjunctive treatment of: fatty liver disease (Tendler et al., 2007); type 1 diabetes (Nielsen, Gando, Joensson, & Paulsson, 2012); type 2 diabetes (W. Yancy, Foy, Chalecki, Vernon, & Westman, 2005); cancer (Fine et al., 2012); and cognitive impairment (Krikorian et al., 2012).
LCHF diets are also likely to be superior to low fat diets for improving several markers of cardiovascular health (Ebbeling et al., 2012; McAuley et al., 2006; Shai et al., 2008) with the possible exception of low density lipoprotein (LDL). However the HDL:triglyceride ratio appears to be more favourably impacted with an LCHF diet in comparison with a higher carbohydrate diet (Sikaris, 2014), and lipid sub-fractions (including large particle LDL) may be increased favourably with an LCHF diet (Westman, Yancy Jr, Olsen, Dudley, & Guyton, 2006).
LCHF diets may provide ‘metabolic advantage’ of greater retention of lean mass, with greater fat-loss when compared to higher carbohydrate diets providing the same amount of calories. This has been demonstrated in short term studies since the 1960s (Benoit, Martin, & Watten, 1965). This does not contravene the laws of energy conservation (first law of thermodynamics) as there are inefficiencies and efficiencies within systems based on macronutrient inputs and the thermic effect of foods of varying macronutrient contents may provide for a net calorie loss (Buchholz & Schoeller, 2004; Feinman & Fine, 2004).
These studies taken in totality suggest that a restriction of carbohydrate, irrespective of what it is replacing has the greatest effect on weight-loss and may positively affect cardiovascular health.
Therefore the position that a higher-carbohydrate diet with low levels of fat is superior for health and thus foods with lower energy, lower fat and higher carbohydrates warrant the Tick is spurious.
The Heart Foundation’s Tick Programme continues to heavily weight against foods containing higher levels of fat and in particular saturated fats despite a paucity of statistical evidence linking reduced fat or reduced saturated fat with cardiovascular disease end points.
A Cochrane Review (Hooper et al., 2011) of RCTs on the effects of modifying fat intake and reduced fat intakes found no overall effect of the diets on total mortality (relative risk 0.98, 95% CI: 0.93 to 1.04) nor CVD mortality (relative risk: 0.94, 95% CI 0.85 to 1.04). However a small relative reduction in cardiovascular events was noted (pooled RR: 0.86, 95% CI 0.77 to 0.96). Other meta-analyses find little statistical evidence for an effect of modified saturated fat intake on CVD mortality (Mente, de Koning, Shannon, & Anand, 2009; Siri-Tarino, Sun, Hu, & Krauss, 2010).
Links between saturated fat intake and CVD end points are primarily found when in modified fat diets, where saturated fat is replaced with another macronutrient, typically either carbohydrate of another fat class (PUFA or MUFA). For example Jakobsen et al. (2009) demonstrated from cohort data a reduction in coronary disease events (pooled hazard ratio 0.69; 95% CI 0.59, 0.81) and coronary disease mortality (pooled hazard ratio 0.57; 95% CI 0.42 to 0.77) when saturated fat was replaced by polyunsaturated fats.
However no association was noted when SFAs were replaced with either MUFAs or carbohydrate, suggesting a positive role in cardio-protection from PUFA intake, and not an absolute effect from the ingestion of SFAs, and casting doubt on the common recommendation to replace saturated fat with carbohydrate and/or MUFAs. More specifically it is suggested that omega 3 PUFAs may be cardio-protective and that this may account for the benefits seen with PUFA for SFA substitution. The meta-analysis by Skeaff and Miller (2009) found that higher intakes of total fat and saturated fat were not significantly associated with CHD in cohort studies, but that various substitutions of PUFA for SFA had beneficial associations in randomised controlled trials (RCTs). However, the strength of results from RCT meta-analysis is highly dependent on selection criteria; inclusion of the Finnish Hospital study (Turpeinen, Pekkarinen, Miettinen, Elosuo, & Paavilainen, 1979), with its unusual “revolving door” methodology and confounding drug use, increases the likelihood of findings favourable to PUFA substitution, while adding the newly recovered data from the Sydney Diet Heart Study has the opposite effect (Ramsden et al., 2013).
Mozaffarian et al.(2010) in a meta-analysis of FA substitution RCTs which also failed to distinguish between omega 6 and omega 3 fatty acids stated that the method “cannot distinguish between potentially distinct benefits of increasing polyunsaturated fatty acids (PUFA) versus decreasing saturated fatty acids (SFA).”
RCTs conducted in the past to test this hypothesis did not produce conclusive results, but were suggestive of benefit from omega 3 fatty acids only (Ramsden et al., 2013). And clinical practice guidelines such as those published by the American College of Cardiology support the use of omega 3 fatty acid supplements for women (Mosca et al., 2004).
A common criticism of higher fat-containing diets is the suggested linear correlation between LDL-cholesterol and ischemic heart disease mortality. However the effect of a distorted HDL-total cholesterol level appears to be a greater factor associated with IHD mortality by a factor of around 40% (Prospective Studies Collaboration, 2007) and diets lower in carbohydrate and higher in fat have consistently demonstrated improved HDL-total cholesterol ratios, along with reduced triacylglycerol levels (Foster et al., 2003; "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," 2003; Sharman et al., 2002; J. W. S. Yancy, Olsen, Guyton, Bakst, & Westman, 2004). More recently Westman and colleagues have evaluated differences in lipid sub-fractions between low-fat and low-carbohydrate, high-fat diets and found reductions in VLDL, medium and small size LDL, increases in large particle LDL although total LDL wasn’t reduced(Westman et al., 2006). A review of RCTs including 447 participants found statistically significant reductions in triglycerides and improved high-density lipoprotein cholesterol in those following LCHF vs LFHC (Total cholesterol and low-density lipoprotein cholesterol values were reduced more in those following LFHC) (Nordmann, Nordmann, Briel, & et al., 2006). Recently Chiu and colleagues have demonstrated no appreciable difference in insulin sensitivity or plasma lipids or lipoproteins related to either saturated fat intake or protein intake in a lower carbohydrate diet (Chiu et al., 2014).
There is little evidence to suggest that saturated fat or total fat intake play a causal role in cardiovascular or other disease and the continued attention that these receive as a result of the existing Heart Tick criteria are providing for confusion in the public and this confusion is not warranted given the existing scientific evidence. Likewise a continued predilection to higher-carbohydrate food type, often of a highly processed and refined nature ignores the role of dysglycaemia, dysregulated insulin response and resultant metabolic disorder that is a co-factor in the development of cardiovascular disorders.
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