If you’ve been following the nutrition news lately, you may have noticed that the question of sugar toxicity is a somewhat polarising one.
Everyone agrees that a massive reduction in fructose (i.e. fruit sugar) does a lot to slow the dramatic rise in obesity and diseases that cluster around the metabolic syndrome.
But, does this mean the rest of the carbs get off the hook?
Dr Robert Lustig, the world’s expert on the perils of fructose who is on the front line of the rising tide of childhood obesity, thinks not.
- Sugar may be more metabolically harmful than simply failing to provide nutrients (if you’ll recall, the “empty calorie” hypothesis is the reason one should limit sugar is because calories from sugar are not as valuable as those from, say, protein).
- Long-term chronic exposure to sugar, similar to alcohol, can be intoxicating and increase risks for diseases that we never used to see in youth prior to 1980.
- As such, sugar should be regulated in a manner commensurate with the damage it causes, possibly as vehemently as alcohol or smoking.
- Evidence is emerging that sugar is addictive and more research needs to be invested in what’s going on chemically in the brain of obese vs lean individuals.
- Industry is capitalising on neuroscience and how cues in our food environment trigger overeating and addiction to drive sales.
Let’s address these points in order.
Sugar toxicity: How does it all begin?
Many studies on the link between sugar and increased risks of heart disease, metabolic syndrome, fatty liver disease or obesity are only describing a temporal association and not a cause-and-effect relationship.
Yet, the evidence is compelling in research studies: When consumed in high amounts and frequently, sugar can be considered a toxin.
In the February 2nd issue of the journal Nature, Dr Lustig and his colleagues argue that excessive consumption of fructose sugar, in particular, can cause many health problems including insulin resistance, dyslipidemia, hypertriglyceridemia, hypertensio, hepatic dysfunction and, of course, the creation of addictive behaviours.
The many links between excess sugar and chronic disease are all exposed on SugarScience.org, a new website and product of Dr. Robert Lustig that uses graphics, videos and science on more than 8,000 independent studies on sugar and its role in heart disease, type 2 diabetes, liver disease and more.
For example, the site reads:
“Over time, consuming large quantities of added sugar can stress and damage critical organs, including the pancreas and liver. When the pancreas, which produces insulin to process sugars, becomes overworked, it can fail to regulate blood sugar properly.
Large doses of the sugar fructose also can overwhelm the liver, which metabolizes fructose. In the process, the liver will convert excess fructose to fat, which is stored in the liver and also released into the bloodstream. This process contributes to key elements of the metabolic syndrome, including high blood fats or triglycerides, high cholesterol, high blood pressure and extra body fat in the form of a sugar belly.”
All of this metabolic mayhem is a breeding ground for diseases afflicting a large part of the population today. Two are of particular concern for Lustig: type 2 diabetes and non-alcoholic fatty liver disease (NAFLD), that the youth are becoming increasingly susceptible to.
The two are actually very interrelated, as the toxicity of sugar is in fact primarily related to its hepatic metabolism, whereby it increases the amount of liver fat and this is one established risk factor for metabolic syndrome and type 2 diabetes.
Case in point, a 2016 paper published in the Journal Nutrients, which looked at dietary habits that are primary contributors to increased hepatic fat content, found that high dietary fructose sugar is strongly associated with NAFLD and NAFLD-related diseases.
In contrast, and perhaps counterintuitively for some, it also points out that high intakes of monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs) exert beneficial effects on NAFLD patients – Another blow to the low-fat dieting camp.
And that’s not all the paper showed. The onset of NAFLD shares some strikingly similar characteristics with those seen in response to a higher-sugar diet, such as elevated insuli, subsequent insulin resistance, unbalanced lipid profile… You name it.
The process by which organs fill up with visceral fat has been described in many studies. It goes something like this:
A healthy person will store excess energy in their fat cells for easy access when required later. But, eventually it gets to the point where they cannot expand to accept any more energy. It is at this point that the fat tissue becomes insulin resistant.
The good news is that insulin resistance will slow the expansion of our fat cells (the excess energy can’t get in as easily). The bad news is that the excess energy will be re-directed for storage into our liver, pancreas, heart, brain and other vital organs.
The parallel between sugar and ethanol
One reason why many experts, like Lustig, thinks we should regulate sugar like alcohol lies in the fact that the metabolic effect of sugar, especially fructose sugar, is nearly identical to that of ethanol from drinking alcohol.
In a recent interview to the website Business Insider, Lustig explains how a growing number of patients – including children – have fatty liver (usually a tell-tale sign of alcoholic liver disease) who rarely drink alcohol, but consume high amounts of sugar.
As it turns out, sugar and alcohol are metabolised virtually identically in the liver. You get alcohol from fermentation of sugar, so it makes sense that when you overload the liver with either one, you get the same diseases.
Both cause problems from chronic toxicity, i.e., drinking/eating a lot of sugar over a long enough period of time. The only difference is that alcohol is also an acute toxi, meaning it is possible to overdose on ethanol.
Now, does the amount matter? Of course it does, sugar health risks are certainly dose-dependent and context-dependent. An insulin resistant person versus an insulin sensitive person won’t metabolise sugar in the same way. What’s toxic to one person may not be toxic to the next. It’s true of most substances, including tobacco, alcohol, cocaine and heroin.
If we were to define chronic toxicity, it is thought of as the ability of a substance to cause harmful effects over an extended period, usually upon repeated or continuous exposure. The point is much smaller doses, if taken repeatedly, are still toxic.
Lustig is the first to acknowledge that fructose, and sugar at large, is harmful at the doses most people are consuming it today. Recommendations for upper limits of added sugar consumption are currently exceeded and by far.
Our consumption of sugar is increasing at a staggering rate and we consume, on average, about four times the amount of sugar today that we did some 40 years ago. The advent of the low-fat craze is partly to blame, as low-fat is almost ubiquitously synonymous with high-sugar.
Going back to the comparison between fructose sugar and alcohol, if we were to put side-by-side the phenomena resulting from either, we would find, as Lustig did, that excessive consumption of fructose can cause many of the same health problems as alcohol (see table below).
The figure speaks for itself and suggests that about two-thirds of health problems that afflicts a heavy drinker also afflicts a heavy consumer of fructose sugar.
If after reading this you’re wondering how much sugar you can eat, it depends on how genetically susceptible you are to its effects and what you are optimising for — short-term pleasure or long-term health.
For some people, eating ten apples a day causes no harm. For others, eating one apple a day causes harm. The goal should ultimately be to figure out what your “toxic” dose is and stay well below it.
As stated by Gary Taubes in a great New York Times article, more research is necessary to establish at what dose sugar start becoming toxic. This supposes longer intervention studies, as sugar can’t be regarded as a chronic toxin after one meal, but after 1,000 meals. So studies have to go on for significantly longer to be meaningful and currently few clinical trials of this kind are supported.
The war on sugar: Have we found the winning strategy?
How do you defeat obesity, type 2 diabetes and fatty liver disease? Just telling people to eat less and exercise more isn’t working. Forecasts suggest that three out of every four British men will be overweight or obese by 2030.
Perhaps, just perhaps, we have ignored a whole ecosystem of issues – our patterns of eating and excess, our poisoned environment — that informs our well-being. Put simply: removing sugar may not by itself halt the advancing flood.
One obvious limitation on the fightback against the damage of sugar is the controversies and misinformation that bedevil the field of nutrition research. The public needs to be better informed about the science of how sugar impacts our health, but weaknesses in clinical trials and observational studies are failing us.
The problem is that the results of these studies, that mostly only establish associations and provide no evidence of causality, are helping identify priorities, guide public health planning, and inform strategies to alter dietary habits and improve health.
Another constraint is that the government has lost credibility with the consumer after condoning the funding of research all the way back to the 1950s that took the blame off sugar, further poisoning nutrition science.
It’s also very difficult to get people to change their diet on a large scale over a long period of time. Proof is this study showing that even if you give people free counseling, advice and a free basket of healthy food every week, it won’t make much of a difference.
So it is likely to require a range of sustained approaches and multiple forms of communication in a process measured in decades rather than months. People also need to be given the impetus, or internal motivators, to change.
But even the, what if we can’t change our food environment that easily? What if the constant temptation that drives unhealthy behaviours is purposefully being imposed on us?
A sugar-coated plot: How industry got us hooked
Although the metabolic aspects of diet, such as changes in calorie expenditure and which fuels are providing calories is important, many experts like Lustig now believe that most of the story of obesity doesn’t have anything to do with that.
It’s mostly about why one chooses certain foods and what are the things in the food environment that are influencing these decisions. And this is not taking place in the muscle or liver, but in the brain.
Why is this important? Because there is a failure to understand the addictive nature of eating in obesity, and neither surgery nor junk food taxes alone can correct addictive eating in some people.
One of the saddest effects of sugar overconsumption that Lustig, who runs the obesity clinic at UCSF Benioff Children’s Hospital, noted is that sugar ramps up brain hormones that tell kids’ bodies they haven’t eaten enough, even as they overeat.
Research has, for example, linked dopamine – a reward neurotransmitter that tells our brains we want more – to addictio, motivatio, and more recently to obesity.
Current evidence suggest that behaviours that release too much dopamine eventually leads to addictio, mostly because dopamine should be in balance with serotoni, the mirror “contentment” neurotransmitter that tells our brains we don’t need any more.
Kevin Hall, a Senior Investigator at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) at the NIH has studied in obese cohorts how this “dopamine effect” on pleasure centres in the brain can be triggered by food and how that may have an addictive effect overtime.
Past studies using neuroimaging techniques showed that the number of dopamine receptors in the brain – the things that dopamine binds to in order to generate a signal – and where they’re located vary in people with addiction and those who are obese.
In his study, Hall used a procedure called a PET (positron emission tomography) sca, where a chemical is injected in the blood and goes to the brain where it binds to these dopamine receptors.
One of the things that he and his team found was that there is a relationship between the binding of these dopamine receptors and key parts of the brain called the dorsal lateral striatum (DSL). These are regions of the brain previously involved or implicated in habitual behaviours.
One hypothesis in neuroscience is that people who have a large number of available receptors in these dopamine regions of the brain are more susceptible to how dopamine is shifting them towards habitual eating behaviour. And, as expected, Hall found that people who had a higher body fat had more dopamine receptors in this particular region of the brain than lean individuals.
We know, for example, in animal models, that if you block dopamine activity, you can block the development of habits because addiction begins when dopamine moves away from the rewards areas of the brain to these habits areas in the DSL.
Hall calls what fires these regions of the brain and motivate food intake surplus “opportunistic eating behaviour”, which can be thought of as cues in the environment like interpersonal influence, being bombarded with food industry marketing and so on.
The other part of Hall’s study that hasn’t come out yet investigates how these dopamine receptors are altered in the reduced carb versus reduced fat diet, as preliminary findings unsurprisingly indicate that they seem to be affected very differently.
All of these scientific discoveries around addictive behaviours and dopamine, like Hall’s, is something that the sugar industry is heavily invested into through the funding of research that helps develop products that are neurochemically addictive. It’s the rise of what’s called “neuromarketing.”
Producers that make these foods study neurophysiology, evolutionary biology and how to make things addictive. They use flavour combinations and pairings to engineer foods that are hyper-palatable and bypass the neuroregulation of appetite.
In that sense, the population-level rise in obesity can be perceived as a natural response to this situation of constant temptation resulting from chemical neurotoxicity following exposure to certain foods. And this in turn shapes our behaviours, behaviours that would later have serious consequences.
How will this story end?
If we’re worried about obesity, maybe it’s time to pay more attention to the environment that’s shaping it, a toxic food environment that is made more toxic by the constant stream of messages to eat more and eat often.
As for the answer to the question of whether sugar is as bad as Lustig claims, studies on longer-term outcomes of different diets are needed. It very well may be true that sugar, because of the unique way in which we metabolise it and at the levels we now consume it, triggers the process that leads to fatty liver, insulin resistance and all that follows.
Some will say that we should never demonise one nutrient. But when that one single nutrient is now in 80 percent of all foods, we do need to look at it. It’s pervaded our entire food supply and could indeed be toxic, but takes years to do damage.
Until long-term studies are done, we won’t know for sure. Barring that kind of study, we have to make the best decisions that we can given the current evidence. Everyone needs to decide how they want to interpret it and make personal choices around it.
Sugar is not solely to blame for obesity and metabolic disorders, there is a host of other factors. But the science is now saying that it is a major player, so there’s no possible risk in lowering sugar intake.