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The sugar debate and nutrition: Obesity and ‘empty calories’

Journal of the New Zealand Medical Association
NZMJ 11 April 2014, Vol 127 No 1392; ISSN 1175 8716 Page 6
The sugar debate and nutrition: obesity and ‘empty calories’
Anne-Thea McGill
There is little doubt that refined high energy food, such as added sugar, contributes to
being overweight.
This is a problem for more than two-thirds of adult New
Zealanders, but also over 20% of children.
United Nations (Food and Agriculture
Organization) data for our country indicates that, on average, we consume about 147
grams per day (37 teaspoons) of added sugar.
However the low quality nutrition or
lack of other micronutrients in these foods may be the greatest health risk—the
‘empty’ part of ‘empty calories’ does matter.
We now have new science information on why we eat so much refined high energy
food and what the metabolism is behind obesity and associated poor health. By briefly
putting the issues together we may be able to see where sugar fits into obesity-related
We, as a society, are still tough on our very overweight members. Embarrassment and
distress is very common in those of us who know we can’t control our body weight
and shape,
and that is most of us. The problem is that the over-appetising, refined
high energy food is so irresistible, and sugar is a major player.
Why have we ‘not
noticed’ how strong the drivers are that make so many of us become obviously
overweight and/or unwell.
Those who put on large amounts of weight in peripheral (hip-thigh-buttock),
subcutaneous areas have problems with moving around/walking,
and psychological
concerns about body shape.
For others, without the capacity for storage in these
lower-body metabolically-safe areas,
‘toxic’ lipids accumulate in organs, such as
liver, and as upper body or central obesity.
The risks for type 2 diabetes, cardiovascular disease, and later-life cancers and
neurodegenerative disease are serious, but even so, changing away from refined
energy rich food patterns is not easy. Whist management of weight loss and/or
metabolic improvement are different for both body types,
managing the desire for
refined high energy food is not.
Sugar addiction has become hard to contest from the extensive literature.
especially combined with starchy, fatty and salty food—activates addiction pathways
in the brain. Drugs of addiction are similar to neurochemicals in the primordial reward
system for acquiring high-energy food.
What’s more, we all really know what these foods are; test question—what foods
would you go down to the local food store for, late at night? Answer—sugary drinks,
confection including ice cream/blocks and chocolate, salty fatty potato chips,
biscuits/crackers with sweet or savoury toppings and other ‘junk food’. Not apples,
not plain cooked meat, and not even sweet dried fruit.
NZMJ 11 April 2014, Vol 127 No 1392; ISSN 1175 8716 Page 7
Many of us know that sometime or other, for health and wellbeing, we will have to
move to a diet without (or with highly controlled allocations of) addictive foods, and
we’ll need help.
Although there have been a great many studies in the last few decades on what foods
cause fat gain, much research did not follow early leads, which in hindsight appear
Sugar addiction and obesity has been mooted since mid-last century.
Lawrence wrote
in 1941 “…animals build up reserves of fat from carbohydrate [sugars and starch] …
‘Diabetic obesity’ is very common … in the earliest stages and again after insulin
The switch to believing that dietary fat caused heart disease seems to have come from
the Seven Countries study. Although some data appeared in 1995,
and methodology
shortcomings were critiqued shortly after,
the main study was published in 1970.
By the early 1980s ‘saturated fat caused atherosclerosis’. Many heart health
guidelines since then advise low saturated fat diets. Recently, it has been shown that
when industrial ‘transfats’ (and non-free range animal fats) are excluded, saturated
fats are not the major contributor to weight gain or metabolic problems,
but that
sugars are.
The upshot was that (refined) carbohydrates were pushed with great haste and vigour
into our processed food supply—they were cheap, already deemed ‘staple’ foods and
in mass production. They are highly palatable in combination (starchy food plus fat)
or easy to hide in other items to ensure purchase (sugar added to drinks or sauces).
Food staples occur in agricultural societies, and are single or few items that are
consumed most days. They are usually easily available, cheap, often storable, and are
usually the major energy supply with variable other nutrients. Staples can be fruit
(coconut, bananas), seed (pulses, grains), roots/tuber (turnip, potato), oil (olive), and
sometimes animals or fish.
We did not evolve with staples, starch or otherwise. Westernised food is probably at
least 72% different from most pre-agricultural forger or Palaeolithic diets.
Prehistoric foods were typically a mix of myriads of useful nutrients from omnivorous
diets. Highly energy-dense food was relatively rare and/or seasonal.
At this point, controversial clinical nutrition points arise that relate to starch. We can
ask ourselves the following. Are there issues with:
(1) Highly bred grain/tuber starch foods becoming staples in our post-agricultural
(10,000 years duration) diets.
(2) Starch, which breaks down into glucose, initially with the salivary enzyme,
amylase, for use by mouth bacteria that can cause caries,
and rapid absorption from
the duodenum into the blood.
(3) The new bit of science that glucose in overload can flow through the polyol
pathway, via fructose and rapidly form liver fat.
4) There being so few studies investigating diets controlling for whole grain alone,
and that one that has been done showed no benefit of added grain,
which is bred
mainly for energy not micronutrients, and
NZMJ 11 April 2014, Vol 127 No 1392; ISSN 1175 8716 Page 8
5) Addiction, with respect to grain/tuber and other concentrated starch?
There is evidence for the above scattered in a wide literature. Compared to lower-fibre
grain-starch foods, higher-fibre grain is associated with fewer heart disease risks.
However, somewhere along the line, high fibre became equated with highly studied
whole grain fibre.
Insoluble (bran) and soluble grain fibres are, of course, carbohydrates, a term that the
food industry uses to confuse. High fibre from fruit and vegetable diets also carries
many micronutrients, but this effect, as opposed to cholesterol absorption and
improved functional bowel health due to purified fibre, is less well differentiated.
The processed food industry has carefully maintained an advertising commentary of
‘high carbohydrate diets are good for you’ and ‘added sugars can be part of a
balanced diet’. The sugar industry lobbies the public health bodies, and are currently
pressing hard to prevent the World Health Organization (WHO) from changing their
advice to ‘added sugar should make up <5%, [not <10%], of dietary energy’.
Meanwhile, the Internet blogs and media reports become a vehicle for ‘mixing and
matching’ all information—research and opinion. Variations of high and low ‘carb’,
fat, protein diets, and variable glycaemic, fat saturation, gluten free, ‘Palaeo’ and
other themed diets, with other camps discussing food addiction are found; all are
trying to make each theory work in our current nutrition environment.
There is a risk of relegating the most topical, interesting theories to this forum, which
includes a very interested public, and declining to air them in well-known journals.
This means that health and medical practitioners, on the ground, will be left trying to
decipher which information is useful to help patients lose weight and improve health.
It appears that neither the researchers/clinicians nor food processing companies really
want to discuss the idea that any food could be addictive. It is hard to come to the
realisation that food, including our refined staples, can be addictive. We thought that
dietary (saturated) fats contributed to problem in cardiovascular (CVD) disease, and
had much evidence to believe that vegetarian-oriented diet was healthy. The inclusion
in all healthy diets of grain/tuber staples (with or without its fibre) was therefore
assumed. Often patients say they eat one-third less food after bariatric surgery, so if
that one-third of omitted items was addictive refined high-energy food, then the main
change to the food supply would be processed food.
All the evidence points to processed food companies understanding and exploiting
addiction to all refined high energy foods. The umbrella term of ‘carbohydrate’, has
become a foil for not having to mention sugar and refined starch. Tobacco and alcohol
marketing ploys of obfuscation, setting up cues and habit formation are not
The success of traditional Mediterranean diet studies—epidemiological and
prospective—on improving health
is unlikely to only be due to polyphenols in olive
oil and wine.
Studies of basic whole food diets, what were once ‘common or
garden’, and all their nutrients, has been seen as too difficult to pursue. However,
there is strong evidence that that human metabolism is particularly geared to use high
food micronutrient diets in a very efficient manner, both for cellular upkeep, repair
and healthy longevity.
NZMJ 11 April 2014, Vol 127 No 1392; ISSN 1175 8716 Page 9
There is now the technology to study thousands of chemicals in the diet, so the ‘thus
far omitted’ studies of controlled whole food diets, from any and all traditional ethnic
backgrounds, could now proceed.
As health professionals, perhaps we can all now begin put the real ‘common sense’
science together, with evidence from evolution, many epidemiological surveys,
thousands of inconclusive studies that did not control for whole food micronutrients,
plenty of negative data from supplement studies,
a few whole food diet studies
the food processing industry.
We then see non-commercial diets which include natural levels of sugars in fruit,
some starch in coloured vegetables, fats and protein in low processed plant and animal
food, are still likely to be the main way to manage our chronic diseases.
It is heartening to see local public health scientists presenting topical research
to the
public recently, which has been picked up by various media.
The mood of the
community is to demand that the processed food industries’ distribution and
marketing of refined, addictive sugary sweetened beverages be decreased through
However, this may be a distraction to the real health disaster that is upon us. The most
pressing problem is the absolute and relative lack of food micronutrients available to
and consumed by those of us who are the developing young, the older and the unwell
in the community. We must attend to the ‘empty’ in empty calories; the serious
gaping hole.
Obesity is usually a micronutrient deficient state, and a marker of serious malnutrition
and metabolic problems.
Neglect in ensuring that high quality food is available to
all, feeds into the perpetration of poverty, and curtails the cognitive, physical and
reproductive potential of upcoming generations.
We cannot wait whilst we negotiate our societies’ addiction to calories. Certainly
whole foods, even raw nuts and dried fruit, are never going to make the easy profits
that processed food companies are used to. Negotiating non-sugar additives in non-
nutritious beverages with processed food marketeers is not the answer.
We can now easily test food for quality, and grade items for food micronutrient to
macronutrient ratios and content, and add terms for non-nutritive additives/toxins.
With such an important issue, is it not timely for processed food producers to be taxed
on low quality food, with poor micronutrient content? Accordingly, perhaps only high
quality food production should attract direct or indirect public-funded subsidies.
It seems ironic with our hugely sophisticated, technological society that we still need
to provide basic nutritious food to our vulnerable and poor; many of whom are
children and mothers.
It seems to me that public health organisations and our community must ensure that,
against every impediment and apparent cost, it returns to basics. We must feed all
children and mothers; at home, at kō hanga reo, at preschool, at school, at work, on
the Marae (Māori meeting house), at church, nutrient rich, palatable, healthy food
irrespective of the energy content—now.
NZMJ 11 April 2014, Vol 127 No 1392; ISSN 1175 8716 Page 10
Competing interests: Nil.
Author information: Anne-Thea McGill, Senior Lecturer, General Practice and
Primary Health Care, School of Population Health, Tamaki Campus, University of
Auckland—and Research Clinician, University of Auckland Human Nutrition Unit,
Mt Eden, Auckland
Correspondence: Dr Anne-Thea McGill, Senior Lecturer, General Practice and
Primary Health Care, School of Population Health, Tamaki Campus, University of
Auckland, Auckland, New Zealand. Fax: +64 (0)9 3737 624 ; email:
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... Reducing the energy dose from sugars to 5% is expected to bring additional positive health effects (Tigerstrom von, 2012;WHO, 2015;WCRFI, 2017). Studies have shown that excessive sugar consumption is associated with obesity, type 2 diabetes, and tooth decay (Ismail, Tanzer, and Dingle, 1997;McGill, 2014;Clifford and Maloney, 2016). A lot of countries around the world have introduced a special sugar tax on sweetened drinks to reduce sugar consumption, others are planning such solutions (APHA, 2012;Falbe et al., 2016;Sánchez-Romero et al., 2016;Thornton, 2017;WHO, 2017;. ...
... Besides, they are often poorer in pro- tective micronutrients (Crovetto, Uauy, Martins, Moubarac, & Monteiro, 2014;Fardet, M ejean, et al., 2017;Louzada et al., 2015a;Martínez Steele et al., 2016;Moubarac, Batal, Louzada, Martinez Steele, & Monteiro, 2016) and energy-rich (calories) derived from sugars, fat (added) in partic- ular. That is why some scientists talk about "empty" calories (McGill, 2014), so "empty" of bioactive protective micronutrients! A Brazilian cross-sectional study has shown that beyond 13% of daily cal- ories from ultraprocessed products the risk of obesity starts to increase sig- nificantly (Louzada, Baraldi, et al., 2015). ...
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BACKGROUND: Observational cohort studies and a secondary prevention trial have shown an inverse association between adherence to the Mediterranean diet and cardiovascular risk. We conducted a randomized trial of this diet pattern for the primary prevention of cardiovascular events. METHODS: In a multicenter trial in Spain, we randomly assigned participants who were at high cardiovascular risk, but with no cardiovascular disease at enrollment, to one of three diets: a Mediterranean diet supplemented with extra-virgin olive oil, a Mediterranean diet supplemented with mixed nuts, or a control diet (advice to reduce dietary fat). Participants received quarterly individual and group educational sessions and, depending on group assignment, free provision of extra-virgin olive oil, mixed nuts, or small nonfood gifts. The primary end point was the rate of major cardiovascular events (myocardial infarction, stroke, or death from cardiovascular causes). On the basis of the results of an interim analysis, the trial was stopped after a median follow-up of 4.8 years. RESULTS: A total of 7447 persons were enrolled (age range, 55 to 80 years); 57% were women. The two Mediterranean-diet groups had good adherence to the intervention, according to self-reported intake and biomarker analyses. A primary end-point event occurred in 288 participants. The multivariable-adjusted hazard ratios were 0.70 (95% confidence interval [CI], 0.54 to 0.92) and 0.72 (95% CI, 0.54 to 0.96) for the group assigned to a Mediterranean diet with extra-virgin olive oil (96 events) and the group assigned to a Mediterranean diet with nuts (83 events), respectively, versus the control group (109 events). No diet-related adverse effects were reported. CONCLUSIONS: Among persons at high cardiovascular risk, a Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced the incidence of major cardiovascular events. (Funded by the Spanish government's Instituto de Salud Carlos III and others; number, ISRCTN35739639.).
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Aging can be viewed as a quasi-programmed phenomenon driven by the overactivation of the nutrient-sensing mTOR gerogene. mTOR-driven aging can be triggered or accelerated by a decline or loss of responsiveness to activation of the energy-sensing protein AMPK, a critical gerosuppressor of mTOR. The occurrence of age-related diseases, therefore, reflects the synergistic interaction between our evolutionary path to sedentarism, which chronically increases a number of mTOR activating gero-promoters (e.g., food, growth factors, cytokines and insulin) and the "defective design" of central metabolic integrators such as mTOR and AMPK. Our laboratories at the Bioactive Food Component Platform in Spain have initiated a systematic approach to molecularly elucidate and clinically explore whether the "xenohormesis hypothesis," which states that stress-induced synthesis of plant polyphenols and many other phytochemicals provides an environmental chemical signature that upregulates stress-resistance pathways in plant consumers, can be explained in terms of the reactivity of the AMPK/mTOR-axis to so-called xenohormetins. Here, we explore the AMPK/mTOR-xenohormetic nature of complex polyphenols naturally present in extra virgin olive oil (EVOO), a pivotal component of the Mediterranean style diet that has been repeatedly associated with a reduction in age-related morbid conditions and longer life expectancy. Using crude EVOO phenolic extracts highly enriched in the secoiridoids oleuropein aglycon and decarboxymethyl oleuropein aglycon, we show for the first time that (1) the anticancer activity of EVOO secoiridoids is related to the activation of anti-aging/cellular stress-like gene signatures, including endoplasmic reticulum (ER) stress and the unfolded protein response, spermidine and polyamine metabolism, sirtuin-1 (SIRT1) and NRF2 signaling; (2) EVOO secoiridoids activate AMPK and suppress crucial genes involved in the Warburg effect and the self-renewal capacity of "immortal" cancer stem cells; (3) EVOO secoiridoids prevent age-related changes in the cell size, morphological heterogeneity, arrayed cell arrangement and senescence-associated β-galactosidase staining of normal diploid human fibroblasts at the end of their proliferative lifespans. EVOO secoiridoids, which provide an effective defense against plant attack by herbivores and pathogens, are bona fide xenohormetins that are able to activate the gerosuppressor AMPK and trigger numerous resveratrol-like anti-aging transcriptomic signatures. As such, EVOO secoiridoids constitute a new family of plant-produced gerosuppressant agents that molecularly "repair" the aimless (and harmful) AMPK/mTOR-driven quasi-program that leads to aging and aging-related diseases, including cancer.
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To summarise evidence on the association between intake of dietary sugars and body weight in adults and children. Systematic review and meta-analysis of randomised controlled trials and prospective cohort studies. OVID Medline, Embase, PubMed, Cumulative Index to Nursing and Allied Health Literature, Scopus, and Web of Science (up to December 2011). Eligible studies reported the intake of total sugars, intake of a component of total sugars, or intake of sugar containing foods or beverages; and at least one measure of body fatness. Minimum duration was two weeks for trials and one year for cohort studies. Trials of weight loss or confounded by additional medical or lifestyle interventions were excluded. Study selection, assessment, validity, data extraction, and analysis were undertaken as specified by the Cochrane Collaboration and the GRADE working group. For trials, we pooled data for weight change using inverse variance models with random effects. We pooled cohort study data where possible to estimate effect sizes, expressed as odds ratios for risk of obesity or β coefficients for change in adiposity per unit of intake. 30 of 7895 trials and 38 of 9445 cohort studies were eligible. In trials of adults with ad libitum diets (that is, with no strict control of food intake), reduced intake of dietary sugars was associated with a decrease in body weight (0.80 kg, 95% confidence interval 0.39 to 1.21; P<0.001); increased sugars intake was associated with a comparable weight increase (0.75 kg, 0.30 to 1.19; P=0.001). Isoenergetic exchange of dietary sugars with other carbohydrates showed no change in body weight (0.04 kg, -0.04 to 0.13). Trials in children, which involved recommendations to reduce intake of sugar sweetened foods and beverages, had low participant compliance to dietary advice; these trials showed no overall change in body weight. However, in relation to intakes of sugar sweetened beverages after one year follow-up in prospective studies, the odds ratio for being overweight or obese increased was 1.55 (1.32 to 1.82) among groups with the highest intake compared with those with the lowest intake. Despite significant heterogeneity in one meta-analysis and potential bias in some trials, sensitivity analyses showed that the trends were consistent and associations remained after these studies were excluded. Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight. The change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes, since isoenergetic exchange of sugars with other carbohydrates was not associated with weight change.
The identification of nutrients and the study of their bioactivity were significant developments in the evolution of contemporary nutrition science. This review argues for shifting the focus towards food in order to better understand the nutrition-health interface. It begins by introducing the concept of food synergy (a perspective that more information can be obtained by looking at foods than at single food components) to denote the action of the food matrix (the composite of naturally occurring food components) on human biological systems. A proposal is then made for the means by which food-focused research might build the knowledge base for etiologic discovery and appropriate dietary advice. The diet-heart disease dilemma is put forward as an example of where a nutrient-based approach has limitations, and a summary of studies targeting food composition strengthens the case for a food-based approach. Finally, the argument is made that evidence from interventions points back to the central position of food in the relationship between nutrition and health, a position that begs for more whole food-based research.
Let’s bust the myth of its role in heart disease Scientists universally accept that trans fats—found in many fast foods, bakery products, and margarines—increase the risk of cardiovascular disease through inflammatory processes.1 But “saturated fat” is another story. The mantra that saturated fat must be removed to reduce the risk of cardiovascular disease has dominated dietary advice and guidelines for almost four decades. Yet scientific evidence shows that this advice has, paradoxically, increased our cardiovascular risks. Furthermore, the government’s obsession with levels of total cholesterol, which has led to the overmedication of millions of people with statins, has diverted our attention from the more egregious risk factor of atherogenic dyslipidaemia. Saturated fat has been demonised ever since Ancel Keys’s landmark “seven countries” study in 1970.2 This concluded that a correlation existed between the incidence of coronary heart disease and total cholesterol concentrations, which then correlated with the proportion of energy provided by saturated fat. But correlation is not causation. Nevertheless, we were advised to cut fat intake to 30% of total energy and saturated fat to 10%.”3 The aspect of dietary saturated fat that is believed to have the greatest influence on cardiovascular risk is elevated concentrations of low density lipoprotein (LDL) cholesterol. Yet the reduction in LDL cholesterol from reducing saturated fat intake seems to be specific to large, buoyant (type A) LDL particles, when in fact it is the small, dense (type B) particles (responsive …
The aetiology of obesity is seemingly simple to understand: individuals consume more energy than they expend, with the excess energy being stored in adipose tissue. Public health campaigns therefore promote dietary restraint and physical exercise, and emphasize individual responsibility for these behaviours. Increasingly, however, researchers are switching from thermodynamic to metabolic models of obesity, thereby clarifying how specific environmental factors promote lipogenesis. Obesity can best be explained not by counting 'calories in and out', but by understanding how specific dietary products and activity behaviours perturb cellular metabolism and promote net lipogenesis. This metabolic approach can furthermore be integrated with more sophisticated models of how commercial practices drive the consumer trends that promote obesogenic behaviours. Notably, obesity treatment has proven more effective if it bypasses individual responsibility, suggesting that a similar approach placing less emphasis on individual responsibility would improve the efficacy of obesity prevention. Successful obesity prevention campaigns are likely to emerge only when the public receive better 'protection' from the commercial practices that are driving the global obesity epidemic. Rather than populations failing to heed governments' public health advice, governments are currently failing the public by abandoning their responsibility for regulating commercial activities.European Journal of Clinical Nutrition advance online publication, 27 February 2013; doi:10.1038/ejcn.2013.31.
Background: Undue influence of body shape or weight on self-evaluation - referred to as overvaluation - is considered a core feature across eating disorders, but is not a diagnostic requirement for binge eating disorder (BED). This study examined the concurrent and predictive significance of overvaluation of shape/weight in obese patients with BED participating in a randomized clinical trial testing cognitive behavioral therapy (CBT) and behavioral weight loss (BWL). Method A total of 90 participants were randomly assigned to 6-month group treatments of CBT or BWL. Assessments were performed at baseline, throughout- and post-treatment, and at 6- and 12-month follow-ups after completing treatments with reliably administered semi-structured interviews and established measures. Results: Participants categorized with overvaluation (n = 52, 58%) versus without overvaluation (n = 38, 42%) did not differ significantly in demographic features (age, gender and ethnicity), psychiatric co-morbidity, body mass index or binge eating frequency. The overvaluation group had significantly greater levels of eating disorder psychopathology and poorer psychological functioning (higher depression and lower self-esteem) than the non-overvaluation group. Overvaluation of shape/weight significantly predicted non-remission from binge eating and higher frequency of binge eating at the 12-month follow-up, even after adjusting for group differences in depression and self-esteem levels. Conclusions: Our findings suggest that overvaluation does not simply reflect concern commensurate with being obese or more frequent binge eating, but also is strongly associated with heightened eating-related psychopathology and psychological distress, and has negative prognostic significance for longer-term treatment outcomes. Overvaluation of shape/weight warrants consideration as a diagnostic specifier for BED as it provides important information about severity and treatment outcome.