Following the established association between higher intake of fruit and vegetables and better health, then many have taken this concept a step further by advocating juicing fruits such that we observe a rise in cafes with large fresh juice bars and expensive juicers being sold commercially to promote this latter concept. Here we will discuss why the reality is opposite to this concept that has been driven by the food & commercial industries and why the juicing process is in fact harmful.
With changing time periods, we have had changing diets and this in turn has caused change in risk factor importance. With the general decline of saturated fats in the diet (see article on dietary fats), the almost abandonment of trans-fat by the process food industry in the UK (by way of legislation), the benefit of unsaturated fat when replacing saturated fats in the diet, then sugar is increasingly regarded as the next villain from the dietary factors. This is particularly more so as replacing saturated fats with carbohydrates (including sugars) does not show the expected benefits. It is important to recognise that from a relative perspective that different risk factors can change over time. Nowadays many people who present with heart attacks are more likely to be overweight and less physically active (thus having features of insulin resistance) compared to the 1970’s.
Carbohydrates can be classed as starch or sugar. Starch is found in most staple foods such as rice, pasta, bread. It is a more complex molecule than sugars and is broken down slowly by digestion and absorbed as glucose but at a relatively slower duration to dietary sugar. This means that the blood glucose increases more slowly, what is termed as relatively “low glycaemic index”, which is good. Starch is best taken as whole grains and not the processed white-type which digests and absorbs quicker. As for dieatary sugar, they are classed as the following;
- Simple sugars (monosaccharides) such as glucose and fructose,
- Compound sugars (disaccharides) such as sucrose (table sugar) and lactose (milk).
- Sucrose (table sugar) is a disaccharide made of one glucose and one fructose molecule, each are metabolised differently.
- Alcohol Sugars such as sorbitol, isomalt, lactitol, maltitol, mannitol, xylitol, glycerol (glycerine) – often used as low calorie alternatives
Free Sugar, Added Sugar & Intrinsic Sugar
That is all nice and good for scientists and students but I find a more useful classification as follows;
- Free sugars which includes Added sugars – those sugars that are added to food (e.g. sucrose, fructose, glucose) or those naturally present in honey, syrups and unsweetened fruit juices.
- Intrinsic sugars – sugar held within the cell structure of food, as in whole fruit and vegetables.
- The rest – this includes lactose in milk, alcohol sugars – we will ignore these for the purpose of this article.
The definitions for ‘Added Sugar’ and ‘Free Sugar’ can vary. Some have defined added sugars as sugars unnaturally added to food and beverages (sucrose sweetened beverages, SSB) but confusingly they include the natural sugars of honey. Some consider fruit juice concentrates within the added sugars definition. Free sugar is defined as added sugar with the addition of fruit juices. But considerable variations remains with in the definition.
The biggest study in the US called NHANES (see later) looked at added sugar where the relative percentage of added sugars in the diets of the U.S. population from ages 2 years and older are shown below. However this study often compared itself to the WHO guidelines which uses free sugars defination. It appears the wording is in essence linked to the region ( i.e US use added sugar definition).
Fruit Juice and Harms of Juicing Process
There is a great difference between intrinsic sugars, which are the sugars locked up inside whole fruits and whole vegetables, than those free sugars in fruit juices. The juicing process that has become a fad should really be regarded as processing, and put alongside other processed food. Juicing has become big business with ever expensive juicers popping up every where and juicing outlets too, looking for the next new recipes on the social media. Unfortunately, I see many newly diagnosed diabetic patients who want to get healthy and due to the widespread mis-information on the internet and social media (at the head of it being promoted by pretend specialist, aka quacks, and those duped by them), that they turn to juicing thinking it will cure them, only to find it make their diabetic control worse.
The reasons for this is three-fold, firstly that the juicing process breaks down many of the cells and releases the sugars that are normally trapped inside allowing for them to be digested and absorbed faster into the blood stream thereby causing a spike in blood sugar (higher glycaemic index). Secondly the soluble and insoluble fibre within whole fruit and whole vegetables helps to slow the absorption of sugars by a gel-like mesh in the intestines however juicing shears the insoluble fibre not allowing this to happen which again causes a bigger spike in the blood sugar. Thirdly, which is also attributed to the main cause of the current obesity epidemic, juices (and other sweetened drink) do not allow the appetite to feel quenched, satisfied and this will cause in some people, particularly if they think it is healthy, to drink more and more juices.
Fructose which is the main sugar present in most fruit juices is accused of many harms too above that of glucose and other sugars, but in the UK most sugars come mixed and so we will leave that topic for another day. But like all things the occasional juice can be incorporated into a healthy diet and it may have some additional benefits for those that don’t eat enough fruit and vegetables. UK guideline allow up to single small glass of fresh juice as part of their 5-a-day of fruit and vegetables. However eating the fruits whole is far healthier as outlined above particularly in those overweight.
Sugar & Body Weight
Historically the recognised harms of excessive sugars were that of weight gain, tooth decay and it was an indicator of poor diet. Overweight and obesity are important risk factors for type 2 diabetes mellitus, cardiovascular disease (heart attacks or strokes), cancer, and premature death as indicated by several studies. The question is whether sugar has an independent effect on these illnesses or whether it occurs through weight gain alone. Historically, it was through weight gain and we will discuss some of the the underlying evidence for this.
The effect of sugar to cause weight gain appears to be through calories alone and not some other unique metabolic pathway as supported by a meta-analysis (of RCTS by Te Morenga et al 2013). They found that adults who were advised to reduce free sugars in the diet without discussing weight and without controlling the total calories (ad libitum diet) resulted in weight loss but not in the clinical trials where calories were controlled (isoenergetic diets). Likewise they found when advised to increase free sugars and calories were not controlled that body weight went up. Importantly when total calories were controlled then no significant change in weight or fatness was seen. Thus implying weight gain is a simple calorie effect. Others have differed with this interpretation due to other factors seen in small studies elsewhere (particularly extremely high doses of fructose) but have not been able to put forth any other credible interpretation for the effect seen. However, there is growing evidence to suggest that free sugar intake maybe an independent risk factor.
Hard end points are the result of studies where that is a reduction in death of major health events. It is what we really want to show from studies rather than other less important markers, which may or may not lead to the longevity or reduced major illness.
The NHANES study (National Health and Nutrition Examination Survey, prospective cohort) suggested that participants in the US who consumed between 10% and 25% added sugar of their total daily calories had a 30% higher risk of death rates from heart attacks and strokes (cardiovascular disease mortality) while for those who consumed 25% or more added sugar of their total daily calories of added-sugar, the relative risk was nearly tripled.
Here weight (BMI), poor diet and many risk factors were adjusted for statistically and although diabetics were excluded at baseline they is no data supplied as to how many later developed diabetes and whether these were adjusted for. It is important to recognise that although observation studies can show a possible relationship they do not prove causation and so the need for further studies particularly randomised control trials, RCTs.
The observed effect of sugar against mortality is ‘J-shaped’ with the main increase of mortality was seen after 15% of consumed sugar which in a 2000-daily calorie diet would be about two cans of cola (280 calories) daily without any other added-sugar. Others are more stringent such as the World Health Organisation, WHO, advising no more than 10% of daily intake from free sugars with a view of working towards below 5%. UK recommendations are informed by the Scientific Advisory Committee on Nutrition (SACN) whose 2015 report advised that free sugars should not exceed 5% of daily energy intake. NHS recommendations are also at 5% mark with this being equivalent to 100 calories daily which is about 5-6 teaspoons of table sugar daily or two-thirds of a can of cola daily. Incidentally, UK figures (2011) show that the average percentage of daily energy intake from free sugars is 11.6% for adults, 15.6% for adolescents, and 14.7% for children.
Most studies look at soft endpoints which are some marker which may or may not improve longevity and reduced illness. It is possible that an intervention causes less inflammation in the body but overall leads to bleeding from the gut thereby killing people. But only this soft marker is looked for and the overal hard endpoint is not measured, as is the case for most dietary sugar clinical trials. Thus the evidence base is relatively weak compared to to dietary fats.
A study (meta-analysis of RCTs by Te Morenga et al 2014) showed that higher intake of free sugar (compared with lower intakes) was associated with increased concentrations of lipids (triglycerides, total and LDL cholesterol), and increased blood pressure when the heart is relaxed (diastolic BP; Systolic BP only significant in studies of a more than 8 weeks duration). Subgroup analyses showed the most marked effect between sugar intake and lipids were in studies that made efforts to ensure an energy balance (isoenergetic diets) and when no difference in weight change was reported. The effect of sugar intake on blood pressure was greatest in trials ≥8 weeks duration (of about 6.9 mm Hg for systolic blood pressure and 5.6 mm Hg for diastolic blood pressure).
In other words, dietary sugar was increasing lipids and blood pressure despite no weight gain thus indicating an independent effect. However one must also consider this effect is accentuated due to a reduction in dietary fats with isoenergetic diets .
Elsewhere sugary drinks (sucrose sweetened beverages SSBs) have shown to cause a number of effects in addition to blood pressure and lipids;
- Inflammatory response in the blood stream, (inflammation is the bodies healing mechanism)
- Insulin resistance (see below),
- Impaired pancreas function (β-cell function wherein insulin is made), and
- An accumulation of fat in and around the liver and intestines [visceral fat – fructose is thought to be the main driver for this. Also visceral fat is thought to be more harmful than external fat (subcutaneous adiposity) with the example of sumo wrestlers given who have little visceral fat, but lots of subcutaneous fat, until they retire from wrestling than die few years later].
However most of the studies involved higher intakes of sugars than usually consumed by everyday people and were relatively short-term. Thus some have question whether this is a true response or an overdose response.
After a meal high in carbohydrates, particularly sugars, insulin is released from the pancreas in order to allow muscle cells to take up the sugar for usage or storage locally. Also the insulin causes the body to store the excess glucose for future usage in the liver and adipose (fat) cells. Insulin resistance occurs when high insulin levels persist over a prolonged period of time causing the body’s own sensitivity to the hormone to be reduced. Historically it was thought to occur mainly as an effect of being overweight (the old paradigm) but as mentioned above there is some growing evidence that excess glucose alone can cause insulin resistance without increase in weight (the new paradigm, this may explain why we still see thin people with new onset type 2 diabetics, although the vast majority are over weight).
Insulin resistance is closely linked with inflammation, which is the body’s attempt to heal itself, with the exact details being unknown but thought to be linked with the release of a chemical called cytokines which subsequently interrupts the action of insulin. Weight gain, particularly around the middle, is likely to be one of the earliest symptoms rather than a cause with the new paradigm of insulin resistance along with other non-specific symptoms of lethargy, hunger, poor concentration and high blood pressure. If left unchecked it will eventually lead to type 2 diabetes mellitus but can take many years or decades to develop.
I have given insulin resistance its own sub heading because of its probable epidemic being associated with the obesity epidemic and likely a precursor to most of the type 2 diabetes mellitus being seen. We will only know for sure if we see a diabetes epidemic for which there are some very early indicators particularly with type 2 diabetes mellitus being diagnosed among children. Even from the heart disease perspective some computer models have suggested insulin resistance as being the most important factor estimated at 42% of cause of coronary heart disease deaths. While looking at it from the angle of insulin resistance (a meta-analysis by Gast et al) has shown that coronary heart disease risk increases by 46% for an increase of 21% for fasting glucose concentration and an increase of 4% for fasting insulin concentration (and an increase of one standard deviation in HOMA-IR concentration).
The evidence base for dietary sugar is a lot weaker than that of saturated fats and more long-term studies looking at hard endpoints of heart disease are needed. There is support to suggest (but not conclusive) that daily diets with 10% to 25% of calories from added-sugar are linked to a 30% higher risk of cardiovascular disease mortality, while diets with calories of more than 25% of added sugar are linked to a tripling of risk. UK guidelines aim for less than 5% of total diet being from free sugars.
There is strong evidence that raised free sugar intake causes an increase in blood pressure and affects blood lipids (cholesterol & triglycerides) particularly more so after 8 weeks duration and is seen the most when weight is stable or even falling while eating the same amount of calories (isoenergetic diets).
Taking extremely high doses of free sugar above that which is consumed by everyday people has a more marked effects in the blood causing inflammation, insulin resistance and reduced pancreas response and accumulation of fat in and around the abdominal organs (called visceral fat).
This is an area that has had an increasing interest over recent years but more data and studies are needed to have a strong evidence-base to advise with. But long-term dietary studies have an inherent difficulty as discussed in Part 1.
Contrary to the statements of some pretend experts (quacks) and those duped by them, eating whole fruit and whole vegetables as are better than juiced free sugars. Some vegetables well be better eaten lightly steamed.
God willing, we will discuss other aspects of high sugar intake particularly the metabolic syndrome in a further article.