Sweet As: The Sugar Trap – And How to Escape It
“Education consists mainly of what we have unlearned.”
– Mark Twain
The following article draws heavily from lectures by Professor Robert Lustig, MD, linked to in the references. As always, readers are invited to draw their own conclusions. Below is what makes sense to me regarding sugar. =)
You likely heard it before: fat doesn’t make fat – sugar does….
And we’ve known this for a while: a low carbohydrate diet successfully helped William Banting reduce his body weight by 46 lbs (from >200 lbs), improving overall wellbeing and reducing health risks associated with obesity: heart disease, arthritis, metabolic syndrome, diabetes, high blood pressure, stroke, and cancer (Diamond 2001). Excited by his results, Banting published his method in a book: “Letter on Corpulence” – a British 1864 bestseller.
A lot of time passed since, and while the basic premise remains, we know in better detail why sugar is detrimental to our health. And not just any sugar, either. In one of his highly recommended presentations (2009), Dr. Robert Lustig, Professor of Pediatrics (Endocrinology) at UC San Francisco, explains in detail the metabolic pathways that lead to physiological problems – a story spanning some 40 years, with Dr John Yudkin, a British nutritionist, the first to point out the devastating effects of refined sugar in his 1972 book “Pure, White, and Deadly”.
Fat versus sugar (or doctrine vs properly presented data)
Similar to butter vs margarine, industrial interests and dirty politics played and play a decisive role in the debate. Sadly, in the end, one always seems to follow the money. Dr Yudkin saw himself viciously attacked and his reputation destroyed for pointing out the truth (Leslie 2016). Both stories share a root in Ancel Keys’ 1950s “Diet Heart Hypothesis” – the idea that consuming animal fat causes heart disease (hence the turn to margarine as butter substitute and the 1980s low fat craze). This “Lipid Hypothesis”, as it is also known, influenced decades of governmental health advice – and thus public perception, opinion, and action. As pointed out in a previous article, however: “[…] one of the central studies purporting the “Lipid Hypothesis” was majorly flawed (Ravnskov 1998, DiNicolantonio 2014). Data were omitted and misrepresented [Lustig 2009, Diamond 2011]. When re-analyzed, trends turned out a lot weaker (Ravnskov 1998). The result: there’s little to no evidence that a high fat diet causes heart disease (Ravnskov 1998, “Fat Head” 2009, Mente et al. 2009, Hite et al. 2010, Diamond 2011, Lundell 2012), and data in support of a low fat diet are lacking (DiNicolantonio 2014). Despite scarce valid evidence for the […] cholesterol story we all know and lots against it and the connection between saturated fat intake and coronary heart disease (Weston A. Price Foundation 2000, Siri-Tarina et al. 2010, Ramsden et al. 2013), the (misinformed) public still thinks of the low-fat diet tale as well established, almost doubtless scientific fact” (Geist 2015).
Yudkin and Keys were contemporaries. Perhaps the available evidence at the time pointed more towards saturated fats as problematic, rather than sugar. Publication of Keys’ Seven Countries Study in 1970 seemingly lent further credence to the idea and – despite other viewpoints – firmly established it in scientific, administrative, and public minds alike. Until its re-analysis by doubting researchers decades later. Yudkin always remained skeptical, as did others in the scientific community, continuing to publish papers showing the (significantly) negative relationship between sugar (not animal fat) consumption and heart disease (Yudkin 1957, 1972). In time, others confirmed his findings (e.g. Kuo & Bassett 1965). Yudkin experienced what Max Planck, the “father of quantum theory” and 1918 Nobel laureate, pointed out in the middle of the last century:
“A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.”
– Max Planck
Meantime, the public avoided saturated fat like the plague and learned to prefer carbohydrates (sugar), led by bad science, big business, and government recommendations. However, instead of becoming healthier by cutting out fat, as one would expect if the lipid hypothesis were correct, we became sicker. And we’re eating more than compared to 30 years ago. In particular, we consume more sugar than ever before, while fat intake decreased and protein uptake remained about the same (Lustig talk 2012). The average U.S. American ingests 22 tsp of sugar a day (WebMD) – instead of the recommended 6 (women & children) to 9 (men) tsp (Lustig talk 2012). One tea spoon approximates 5 g.
Less fat and more refined sugar equals an increasingly sick populace (Lustig talk 2009). That’s the current public health perspective and the result of c. 40 years of dietary guideline mismanagement, beginning with Ancel Keys, the doctrine of his lipid hypothesis in the 1950s and its far reaching downstream consequences, enacted by legislators, adapted to by the food industry, and endorsed by citizen’s groups in the US and elsewhere.
“A generation of citizens has grown up since the Diet/Heart hypothesis was launched as official dogma. They have been misled by the greatest scientific deception of our times: the notion that consumption of animal fat causes heart disease.”
– Prof George Mann, MD
Why we like sugar
In evolutionary terms, we’re hardwired to liking sugar, because no natural sweet food is acutely poisonous. Good to know – and we do. The food industry, however, does too. We like sweets because they offer the body easy access to sugar – its main fuel. Thus, it needn’t expend extra energy to break down long carbohydrate chains to excise simple sugars – they’re already short and readily absorbed at consumption. One could say the food industry successfully hijacked this instinct by adding sugar to most any product – about 80% of today’s c. 600 000 supermarket items contain it (Enders 2015). And not only that: turns out sugar is addictive. According to Dr Mark Hyman (Origin film), eight times more so than cocaine. Like a drug and unlike natural foods, refined sugar stimulates a repeated dopamine release in the reward center of the brain (dopamine is part of the brain’s “Feels good, let’s have it again!” response).
“The rapidly increasing rates of obesity, combined with the high failure rates of obesity treatment, has led to the hypothesis that ultra-processed foods (often high in sugar) may be capable of triggering an addictive process.”
– Gearhardt, Roberts & Ashe (2013)
Evidence backing the above quote is accumulating from both animal and human studies (e.g. Wideman et al. 2005, Rada et al. 2005, Lustig 2010, Zhen et al. 2011, Lustig talk 2012, Avena et al. 2015, Shariff et al. 2016).
To understand the effect of sugar on our body, let’s revisit how fat and sugar interplay in our physiology. You will also see that sugar is not sugar – its source and molecular structure matter a great deal to us, affecting very different metabolic outcomes (Jastreboff et al. 2016).
What happens to fat and sugar after ingestion?
Fat – What is it? Why do we need it? What does the body do with it?
Fat, together with sugar and protein, is a fundamental building block of biology. It yields twice as much energy compared to sugar. We must derive essential fatty acids (omega 3 & 6) from our diet.
Fats ensure proper brain function (our brain consists of 60% fat), help carry, absorb and store fat-soluble vitamins (A, D, E, K), provide fuel and energy storage, and constitute the fundamental cell membrane component, among many other important functions. We need fats to maintain cellular health. A low fat diet is a disaster for our brain (Dr Daniel Amen, Origin film).
As fat is not water soluble, the small intestine largely leaves dealing with it to the lymphatic system, which pools, transports, and releases consumed fats as triglycerides into the venous blood stream, where they eventually reach the liver. Subsequently, fats either fuel cellular energy generation straight away, or become part of fat depots to await later use. Far from just serving as dumping ground for excess calories and toxins, fat tissues cushion organs and provide an energy supply for the body when glucose runs low (e.g. between meals or during fasting).
Sugar – What is it? Why do we need it? What does the body do with it?
Sugar is a carbohydrate energy source (not a nutrient). The body runs on glucose, a simple sugar (Fig. 1). Sugar reserves last for about a day and the body can manufacture its own glucose – there’s absolutely no need for adding sugar to anything in our diet to fulfill physiological demand. Our brain relies heavily on glucose, as do our red blood cells. Both require regular amounts, as amply present in whole foods (e.g. fruit & vegetables). All cells in the body know how to use glucose – it’s a universal currency of our physiology. Indeed, of life itself – most life forms use it. Plants build it from light, water, and CO2 (photosynthesis) and store it as starch (e.g. potatoes, carrots). Animals break down starch into glucose when eating plants. Glucose is familiar everywhere.
When lots of glucose enters the system, liver and muscles store most as glycogen, the animal equivalent to plant starch. When glycogen stores fill up, the liver converts sugar to fat. Note that sugar can convert to fat, but not the reverse – the reason why added sugar literally makes fat.
Essentially, sugar fuels cells by metabolizing to ATP, an energy-rich molecule that supports a myriad of cellular processes, and without which you and I wouldn’t exist.
So far, so good – but not all sugars are equal.
Glucose vs fructose metabolism in relation to metabolic syndrome
Contrary to glucose, which all cells readily recognize, only the liver metabolizes fructose. Like glucose, fructose is a simple sugar (Fig. 1). Combining the two yields sucrose, or table sugar. The liver processes all incoming fructose and only about 20% of consumed glucose (as other cells also use it, and it never reaches the liver). So the sugar source matters: fructose creates a much larger burden on the liver compared to glucose. The two also metabolize differently, which matters a great deal to your liver and your health.
Among many other pathways, our energy balance involves the hormones leptin and insulin. When a meal comes in, energy stores replenish, fat cells release leptin, and that signal communicates our satiety status to the brain, which in turn tells the body to ease off appetite and food intake. Leptin decreases appetite. Insulin works in two ways: it tells the body to use sugar for fuel instead of fat, and it communicates to the brain “stop eating, we’ve got enough to deal with at present”. So it, too, forms part of the satiety feedback loop updating the brain on our “fullness status”. Insulin originates in the pancreas and aids glucose enter into cells. Consequently, blood sugar levels decrease. Insulin is the only hormone that can reduce blood glucose levels.
While cellular glucose uptake depends on insulin, fructose does not. It uses a different mechanism. It bypasses the insulin satiety signal to the brain and we literally don’t know that we ate fructose. The liver turns large amounts of dietary fructose into fatty acids (de novo lipogenesis), which either release into the blood stream as triglycerides, or remain in the liver or in fat tissues as depots. In healthy people, about 30% of fructose metabolize to fat (Lustig talk 2009). A large fructose intake also interferes with the leptin satiety feedback loop and results in overeating because the “fullness” signal to slow and stop food intake disrupts: we keep eating beyond satisfying physiological demand because neither the insulin nor the leptin satiety signal tells us to stop.
Fructose throws the body’s appetite control system out of balance. It induces insulin resistance (see Box 1), which in turn induces leptin resistance (defects in leptin signaling and transport). One could say that obesity is leptin resistance: a situation where the brain doesn’t “see” the leptin signal – and thinks it’s starving – no matter how full the fat stores are (and irrespective of how much leptin they release). Thus, the brain keeps the body eating and conserving energy by remaining largely inactive (“couch potato” state). Consequently, a person gains weight. The paradox is that obese people starve from the inside, due to their imbalanced biochemistry. They don’t feel satisfied despite being overfull. They’re not fat because of couch potato-dom, but rather, they are overeating and sedentary because they are fat, and getting fatter (Taubes 2011).
On top of this, insulin suppresses fat lysis. While its lack results in fat dissolving, chronically elevated insulin levels, cause fat cells to retain their fat. Consequently, the body suffers: insulin resistance, obesity, metabolic syndrome (Box 1), diabetes, dementia, and others. And according to Dr Lustig, “we’re all hyperinsulinaemic now”: compared to previous decades (spanning 40 years), today’s populace shows a 2-4 fold increase in insulin levels (Lustig talk 2014).
Fructose metabolism in the liver also produces uric acid, a compound causing gout and high blood pressure (Lustig talk 2009). Not only that, but liver processing of fructose parallels that of ethanol (alcohol) (Lustig 2010). We know that alcohol can act as an acute and addictive toxin – hence its regulation. Should refined sugar with its slower, yet severe health consequences through constant, chronic exposure receive similar legal treatment?
“Thus, fructose ingestion elicits an endocrine profile that could potentially favor increased energy intake and weight gain by attenuating levels of insulin and leptin, two hormones that inhibit food intake and contribute to the long-term regulation of
energy balance and body adiposity through actions in the central nervous system.”
– Teff et al. (2009)
Where’s the sugar?
According to Dr Lustig, soda, coke, energy drinks, and fruit drinks make up c. 33% of extra sugar sources. Others: salad dressing, barbecue sauce, breakfast cereal, hamburger buns & meat, yogurt, soups, breads, canned & jarred goods – again, some 80% of supermarket items contain added sugar (sucrose, HFCS). See also Dr Mercola’s infographic fructose overload.
High fructose corn syrup
High fructose corn syrup (HFCS) deserves special mention. In essence, this is pure sugar (sucrose) (Fig. 1). Sucrose and HFCS only slightly differ in the ratio of glucose to fructose: sucrose contains 50% fructose. HCFS contains 42-55% fructose. The rest is glucose. That’s it.
According to Dr Lustig (2009 talk), soft drinks and fruit drinks cause type 2 diabetes (Basu et al. 2013) (even though industry would have us believe otherwise (Brackett 2008). What do these beverages contain? HFCS. It is estimated that the average US American consumes about 63 pounds of HFCS annually – is it any wonder this should have personal and national health consequences? A study published in the Journal of Clinical Endocrinology and Metabolism found that obese people who drank a fructose-sweetened beverage with a meal showed triglyceride levels almost 200% higher than those who drank an equivalent glucose-sweetened beverage (Teff et al. 2009). The same authors note that “circulating TG [triglyceride] concentrations were substantially elevated over a 24-h period in normal-weight, healthy women after consumption of fructose-sweetened beverages compared with isocaloric glucose-sweetened beverages, ingested with mixed nutrient meals” (Teff et al. 2004). While healthy people revert back to normal eventually, chronic high triglycerides may be a sign of metabolic syndrome or translate into heart disease (Web MD).
Unfortunately, it does not end there: HFCS is almost ubiquitous in the supermarket foodscape…as a dirt cheap sugar substitute, it found its way into most anything that requires a shelf life and/or needed to be palatable after regulators sought to decrease fat content (in line with lipid hypothesis doctrine). And things without fat taste like cardboard. So the food industry sugared it up a bit. A lot. With sucrose or HFCS in next to everything. Out of 32 types of bread only one did not contain HFCS, for example (Lustig talk 2013). A local supermarket visit turned out an added sugar content between 0g (one item) and 6g per slice of bread, comparing some 15 brands. One reason I happily bake my own rye loaf.
Since sugar and HFCS enjoyed bad press for a while, the food industry adapted by renaming them… different labels, same damage. For example, what do you get when evaporating cane juice? Could it be sugar crystals? Yes. According to Lustig (2013), 30% of items in US supermarkets are misbranded, meaning they give a label not sanctioned by the FDA (US Food & Drug Administration) to avoid the words “HCFS” or “sugar” – hence, the “evaporated cane juice” or “corn sugar” workarounds. Box 2 gives more examples of different guises of HFCS and sugar – all words mean two things: lots of sugar, best avoided.
As a last side note, in 2009 studies found detectable mercury levels in HFCS (Washington Post 2009). Mercury is a neurotoxin. Whether or not it’s still an issue with producing HFCS, I do not know. For other possible consequences of fructose over-consumption, read this (“Other Concerns about HFCS” subheading).
A calorie is NOT a calorie…
“It does not matter where the calories come from, it’s still the same amount, whether originating from fruit, cake, or a soft drink.” This sentiment is equivalent to “fat makes fat” and “cholesterol is bad for you”. All statements lead astray, causing misguided consumer behavior to this day. Old myths die hard – especially when serving enormous financial interests. And food stocks continually perform above the S&P500 (Lustig talk 2012).
Contrary to what Coca-Cola wants you to believe (Fig. 2), research data oppose marketing tricks: a calorie is not a calorie. Some calories cause disease more than others because they metabolize differently, as seen with sucrose & starch (Kuo & Bassett 1965) and glucose & fructose: when you consume 120 calories of glucose, less than one calorie stores as fat. Compare that to fructose, where 40 calories end up as body fat! A factor of 40 difference (Lustig talk 2009). So sugar is not sugar, and a calorie is not a calorie, either. Eating fructose translates into belly fat. Next time you put that white sugar cube into your coffee, imagine a fat blob instead…or watch this…it illustrates what you really do when eating excess sugar….as seemingly little as one can of soda (with its HFCS) a day adds mightily to your belly fat: if consumed daily, that can of soda translates into 15 pounds of fat per year. On average, however, US Americans drink 2.5 cans of soda per day (Lustig talk 2013). And for any extra 150 kcal people in any country consumed per day, diabetes prevalence increased by 1.1% – IF that 150 kcal came from a can of soda (Basu et al. 2013).
“Our results show that sugar availability is a significant statistical
determinant of diabetes prevalence rates worldwide.”
Basu et al. (2013)
Above quote comes from a study that provides causational data for diabetes. The authors estimate that 25% of diabetes worldwide is explained by sugar alone (not total calories, obesity, other food stuffs, or other confounders). Changes in sugar availability predicted changes in diabetes prevalence. Whenever sugar availability changed in any country, diabetes followed by three years. While causation is not yet shown for cancer and dementia, correlation exists, and any cancer patient would be well advised to avoid sugar.
According to Dr Lustig, we now have the same level of causal medical inference for sugar inducing diabetes, heart disease, fatty liver disease, and tooth decay that we have for tobacco leading to lung cancer. Sugar shows a dose-dependent, exposure dependent, directional relationship: the more sugar, the sicker the populace. Fig. 3 exemplifies this with respect to raised blood triglyceride and cholesterol levels in response to sugar (Diamond 2011) – note these data are from 1965. For diabetes, take out the sugar, and its prevalence declines. Reintroduce sugar, diabetes prevalence increases – similar to Fig. 3, just on a population level, analyzing world wide data (Lustig talk 2013, Basu et al. 2013).
Trans-fats, fructose, ethanol, and certain amino acids all bypass the insulin regulated pathways, thus contributing to metabolic syndrome in the same way: overwhelmed liver mitochondria (organelles that produce energy) turn excess metabolites into fat. Liver fat drives chronic metabolic disease. Instead of glycogen storage, as resulting from glucose metabolism, processing above substances largely results in fat deposits, ultimately overtaxing the liver. A calorie is not a calorie. Foods may be isocaloric (containing the same amount of calories), but not isometabolic (they process completely different, thus either contributing to a healthy or a sick biology) (Lustig talk 2014a).
Natural fructose vs added sugar and the adulteration of our food supply
This is not to vilify fructose. It’s a natural sugar and as such poses little risk. Why? It’s a function of amount and form. Fruit may contain lots of fructose, but the accompanying fiber, minerals, enzymes, and other constituents balance it out. An apple a day does keep the doctor away. Rather, it’s sugar in isolation and excess that causes illness. When sourced from fruit and vegetables alone, we ingest about 15 g (~ 3 tsp) of fructose a day. No worries. The excess 73 g a day we currently see adolescents consume (Lustig 2010), stemming from sugar additives to foods already stripped off their fiber and nutritious value, pose the challenge. Real food consists of little sugar and lots of fiber. Processed food contains no fiber and lots of sugar (Lustig talk 2012). That’s the problem. The adulteration of our food supply involves adding fructose and trans-fats, and removing fiber. Not to mention pesticides, fungicides, herbicides, hormones, antibiotics, and genetically modified organisms (GMOs) and their ongoing labeling battle – if it’s so good for us, why fear declaring it? Did you know that only 10 corporations orchestrate our entire processed food supply (Fig. 4)?
Marketing, media & money
And TV advertising does not help: this is where children see colorful commercials on food hardly worth calling it that, which unduly influences their desire, biochemistry, behavior and life, subsequently filling doctor’s offices with conditions of epic proportions as now seen with the obesity pandemic and its metabolic knock-on effects – including obese infants and a 30% increase of type 2 diabetes in children within the last five years (Lustig talk 2014). Nobody wins in this scenario – except food and drug manufacturers, TV stations (paid by food and drug manufacturers) and MDs treating the resulting metabolic mess. Too many parties earn a living from sickness. Too many scientists, regulatory bodies, and MDs are bought by industry (Moynihan & Cassels 2005, Davis 2012, Lustig talk 2014a). The ones that aren’t – like Dr Lustig and many other well meaning practitioners dedicated to their patients – need our help in bringing about change. If the masses ignore the (false) messages and learn what makes good health, all benefit. Selecting one’s truth provider carefully indeed pays. Begin by throwing out your TV…? I did 15 years ago and have never looked back. Magnificent riddance, freeing up lots of time for creative use by yourself or with family and friends. =)
More likely, this pandemic – 75% of the US healthcare budget flow into metabolic syndrome associated illnesses (e.g. diabetes alone cost US $245 billion in 2012, says Dr Lustig) – calls for political, regulatory measures, as with alcohol, drugs, and tobacco. Common sense, education, and personal responsibility aren’t enough. A shopping environment where 80% of foods contain added sugar does little to enable weaning ourselves from a habituating, addictive substance that slowly causes chronic damage. People need appropriate support and society constructive, healthful regulations to prevent a sweeter, fatter future. Who would have thought.
Adjusting to the situation
Obvious solution: shopping consciously, reading labels, and understanding them. It’s our health, and nobody else cares about it as much as we do – least of which, the food industry. The less added (refined) sugar you eat, the happier you liver is and the healthier you are. A good rule of thumb that I follow is: if it has more than one number, it stays on the shelf – saves looking up numbers. While not all stand for undesirable compounds, most do.
With sugar, cooking from scratch avoids its source from many cans and jars. According to Dr Lustig, one should consume less than 6 tsp of sugar per day. One 400g can of organic tomatoes informs me that it contains about 16 g of sugar – c. 3 tsp! While I would rarely think to eat 6 tsp of obvious sugar (e.g. chocolate, cookies, cake) a day, hidden sugars add up rather quickly! So it pays to check labels, adjust what we buy, and rethink how we prepare meals.
Better still: growing our own food. While this is doubtlessly more difficult in big cities, the concept of edible parks flourishes in places – an excellent trend. And it’s surprising what one can grow on a balcony and window sill. Even if it’s “just” herbs: they are very potent and a fresh, healthy and wholesome addition to your meal. They won’t solve the larger issue, but they’ll nourish your body regardless.
Farmers markets and buying organic wherever possible. If one can buy 1 snickers bar, 1 bag of doritos, and 1 60 oz (!) coke for 99c in Texas, then it’s up to us to resist that temptation and turn our back on frankenfood offers like this. What this really promotes is a hospital bed downstream, if consumed regularly. The metabolic syndrome pandemic rages as we speak, and anyone who’s not participating in it by taking their health into their own hands as best they can contributes to a healthier future for all – not to mention feeling better. This sentence is not to be misunderstood as blaming ill people – it simply says that health matters and is up to us, as industries do not have our best interest in mind. We do. Above purchase translates into 112 pounds of fat per year, if consumed daily (Lustig talk 2009). Who needs that? Eating real food is the solution. Above investment of 99c is the worst anyone can make. Even eating nothing is much better than that.
Turns out, a high sugar diet is the high fat diet we were told to avoid for decades: fructose negatively affects the liver, causes inflammation, shows addictive qualities and drives excess food consumption, leading to increased belly fat, weight gain, insulin resistance and its physiological knock-on effects collectively summarized as the “metabolic syndrome”, which swallows up 75% of the US healthcare budget.
“Current fructose consumption has incrementally increased
fivefold in the last century and doubled in the last 30 years.”
– Prof Robert Lustig, MD
Our food supply is largely “fructosified”. Since about 80% of supermarket items contain added sugar, the art of shopping is finding the products without it, shop elsewhere altogether – or grow our own vegetables.
The obesity/ metabolic syndrome pandemic is just that: everywhere. It’s a global issue. Without a doubt, regulators need to step in here. Question is: how long would you like to wait to see that happen? For trans-fats to ever so slowly leave our food supply, it took 25 years. For smoking, it took over 50 years to acknowledge its detrimental effects, force the industry into proper labeling, establish a regulatory framework and ban cigarette advertising (Mercola 2010a, Wikipedia). Better slow than never, but – I don’t have decades to wait until sugar is regulated properly, if ever. This must either happen faster in a top-down manner through the law, or in bottom up fashion, where people leave processed foods on the shelf. Or both.
At the moment, where industry and its supposed regulators are still in cahoots, and effective changes will likely take some time, the best counteraction seems to be to vote with our forks and dollars. To literally ignore the supermarket and fast food foodscapes and opt for real, healthy food. Unfortunately, that’s easier said than done for many people. City dwellers and people in lower income brackets don’t necessarily readily have access to a garden or organic markets. Those most prone to suffering the consequences from our adulterated foodscape are also those who can least afford the alternatives. One reason I appreciate the edible parks concept very much. This certainly is a viable solution which can benefit entire neighborhoods and communities – and it can start now (and has in places). While certainly a very necessary step, waiting for policy to change and force industries into compliance could be like waiting for Godot – he may never come in our life time. Thus, for now, it’s up to us to choose wisely.
The science is in. Below quote describes what happened before when basing health policy on a few charismatic, influential people and their flawed expertise (lipid hypothesis). Are we going to prefer sound science this time, and act accordingly? Or will we bow to industry and its interests once more, deferring and delaying appropriate measures yet again?
“This makes scientific inquiry prone to the eternal rules of human social life: deference to the charismatic, herding towards majority opinion, punishment for deviance, and intense discomfort with admitting to error. Of course, such tendencies are precisely what the scientific method was invented to correct for, and over the long run, it does a good job of it. In the long run, however, we’re all dead, quite possibly sooner than we would be if we hadn’t been following a diet based on poor advice.” – Ian Leslie (2016)
Please note: this article does not constitute medical advice in any way and serves educational purposes only. Each person takes full responsibility for their wellbeing choices and decisions.
Avena NM, Potenza MN and MS Gold (2015). Why Are We Consuming So Much Sugar Despite Knowing Too Much Can Harm Us?
Brackett R (2008). High-Fructose Corn Syrup. A guide for consumers, policymakers and the media. Grocery Manufacturers Association, GMA – Science Policy Paper
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Enders G (2015). Darm mit Charme
Enders G (2015). Gut: The inside story of our body’s most underrated organ
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Lustig R, MD
Talks on YouTube:
Sugar: no ordinary commodity (2012)
Sugar: the bitter truth (2009)
Mann G (1985). Coronary Heart Disease – Doing the Wrong Things
Mercola J (2010). Sugar May Be Bad, But This Sweetener Called Fructose Is Far More Deadly
Mercola J (2010a). Are cell phones the new cigarettes?
Moynihan R and A Cassels (2005). Selling sickness – how drug companies are turning us all into patients.
Rada P, Avena NM and BG Hoebel (2015). DAILY BINGEING ON SUGAR REPEATEDLY RELEASES DOPAMINE IN THE ACCUMBENS SHELL
Shariff et al. (2016). Neuronal Nicotinic Acetylcholine Receptor Modulators Reduce Sugar Intake
Taubes G (2016). The Case Against Sugar
Taubes G (2011). Why We Get Fat: And What to Do About It
Teff et al (2009). Endocrine and Metabolic Effects of Consuming Fructose- and Glucose-Sweetened Beverages with Meals in Obese Men and Women: Influence of Insulin Resistance on Plasma Triglyceride Responses
Washington Post (2009). Study Finds High-Fructose Corn Syrup Contains Mercury
Wideman CH, Nadzam GR and HM Murphy (2005). Implications of an animal model of sugar addiction, withdrawal and relapse for human health.
Wikipedia: Tobacco advertising
Yudkin J (1957). Diet and coronary thrombosis: hypothesis and fact. The Lancet.
Yudkin J (1972). Pure, White, and Deadly.
Zhen C, Wohlgenant MK, Karns S and P Kaufman (2011). HABIT FORMATION AND DEMAND FOR SUGAR-SWEETENED BEVERAGES