A review by Professor Robert Thomas and Kristina Kis of the emerging link between processed sugar intake, processed carbohydrates, high glycaemic index foods and cancer; and how the habit of eating or drinking processed sugar or refined carbohydrates is unhealthy and excess can lead to cancer.
Processed sugar intake and cancer
There remains considerable confusion in the media and debate among health professionals regarding the link between high processed sugar intake and the higher risk of cancer but the evidence is becoming increasingly concerning.
The misunderstanding arises, in our opinion, mainly because most faultfinders of this association fail to emphasise that it’s not sugar itself which is harmful, it’s the habit of eating or drinking processed sugar and refined carbohydrates which is unhealthy. Normal levels of sugar in our blood stream do not cause or promote cancer, it helps to feed every cell in the body, along with other energy sources such as fatty acids and ketones. In fact, sugar is so important to the function of the brain and other organs that the body has several back up strategies to keep blood sugar levels high enough.
Processed sugar and to lesser extent processed carbohydrates are harmful because they lead to inappropriately raised blood sugar levels after eating due to their high glycaemic index (GI). Foods with a high GI, ranked on a scale from 0 to 100 by the World Health Organisation (WHO), cause marked fluctuation in blood sugar levels because they are rapidly digested and absorbed which trigger a rapid insulin response. On the other hand, low GI foods, by virtue of their slow digestion and absorption, produce gradual rises in blood sugar and insulin levels. In addition, the addictive nature of sugary foods and drinks mean they tend to be eaten in excess increasing the glycaemic load (GL) of meals or snacks, a term, which takes into account the amount, as well as the type of food eaten (DiMeglio). Over-eating high calorific foods particularly those rich in sugar increases the risk of metabolic syndrome which is defined by the Adult Treatment Panel III criteria as a combination of abdominal obesity, high triglyceride and hyperglycaemia. This combination leads to a higher risk of insulin resistance, diabetes, heart disease, cancer, dementia and stroke (Basaria, Giovannucci). The worse culprits are free simple sugars added to food or drinks but processed carbohydrates with the bulk removed to increase their GI can be harmful although they more difficult to identify when choosing healthy dietary options.
Types and sources of common sugars and carbohydrates
Carbohydrates, or saccharides using their scientific name, are molecules consisting of rings of carbon, hydrogen and hydrogen atoms. They are important sources of energy for the body and are divided into four main chemical groups in order of size and complexity:
Monosaccharides: Glucose, fructose, galactose and xylose. The later two are rarely found naturally on their own but some amounts of free natural glucose can be found in figs, sweet corn, grapes, mango and bananas. Fructose is more commonly found in fruit such as, apples, fig, grapes, pears, honey and some root vegetables. The vast majority of glucose and fructose we eat is added by the manufacture, chief or consume
Disaccharides: Sucrose (a fusion of glucose and fructose) is the main component of table sugar It is the usual sugar added to sweets, candies, sugary drinks, toffees, pastries, cakes, donuts and processed foods. Sucrose is harvested from sugar cane or sugar beat. Lactose (glucose and galactose) is the common sugar found in milk. People with lactose intolerance lack the enzyme, in the gut, which breaks down the bond between glucose and galactose to enable its absorption. Maltose (glucose and glucose) found in malted drinks, beer and can be found naturally in cereals.
Oligosaccharides: These are intermediate chain carbohydrates found in artichoke, burdock, chicory, leeks, asparagus and onions. They are commonly used as food additives as the give food and drinks a smooth more substantial texture. The most commonly used oligosaccharide additives include maltodextrins, inulin and oligo-fructose. They are sometimes referred to as soluble fibre or prebiotics because they are not easily broken down in the small bowel and 90% pass to the large bowel providing energy for the commensal bacteria. As a consequence, certainly in their natural forms they generally regarded as healthy [ref.
Polysaccharides: Starch, amylose, cellulose and pectins. Starch is the most common carbohydrate in the human diet and is contained in many staple foods. The major sources of starch are cereals (rice, wheat, maize, oats, millet, barley) and any foods made from them such as bread, pasta, chips, cakes and noodles. They are also found in root vegetables such as potatoes, carrots, cassava, swede, sweet potato, yams and legumes (beans, lentils, soy, peanuts, beans, peas). These complex polysaccharide-containing foods, in their natural form, tend to contain other nutrients such as fibre, proteins, vitamins and minerals which are not only are healthy for the body they slow the transit of the food through the gut, slowing the stomach emptying time delaying the break down and absorption of glucose. Unfortunately, processing these foods often removes many of these healthy elements and increases their breakdown and absorption times thus increasing their GI.
Fructose versus glucose: Another common misconception is that fructose has less of a negative impact on the body than glucose. This confusion probably arises because fructose is the most common sugar in fruit, which have numerous other nutritional benefits. The other issue is that fructose unlike glucose is less likely to trigger an insulin increase, as it is not required for its metabolism. Unfortunately, excess fructose intake is just as harmful. In one laboratory experiment, rhesus monkeys feed a, human-like, high fructose diet developed diabetes within 3 months (Bremer). In humans, even after 4 weeks of a high processed fructose diet signs of insulin resistance appeared (Silbernagel) and several other studies have linked a high fructose diets (>50g/day) with hypertension, obesity, the metabolic syndrome (Johnson, Livesey) raised uric acid and type 2 diabetes (Johnson).
Fructose in whole fruits: In must be emphasized that although low amounts of fructose in present in whole fruit, no study has shown that eating a lot of fruit is harmful – in fact, quite the opposite, people who eat ample daily fruit are usually healthy (Song, Thompson Xiao). There are several reasons for this disparity. Compared to adding processes sugar to foods, the table below shows the levels of sugar in whole fruit is still relatively small, even with those with the highest concentrations such as grapes, mango and pomegranate. At these concentrates it would near impossible to get to harmful levels of fructose by eating whole fruit. The fibre and pulp makes fruit satiating deterring the individual from eating other foods because they feel full. The pulp and fibre also make it harder to digest slowing down gastric emptying and thus reducing the GI. Whole fruit is also rich in vitamins, minerals and healthy phytochemicals all of which help the body in many ways including fighting cancer. That said, there are a number of ways humans have managed to make fruit potentially unhealthy:
Dried fruit: The process of drying and processing the fruit removes water and damages some of the nutrients but more importantly significantly concentrates the fructose content. Some manufacturers also add more sugar and sulphites as for taste and preservation. The table below show the x5-x6 fold increase in sugar by this process (eg fresh figs-7% dried figs-55%). On the positive side however, despite this high in sugar content, they still have their fibre, polyphenols and pulp so their GI is still lower than an equivalent processed food with similar levels of sugar.
Fruit juices: Many of the fruit juices on the market aren’t even “real” fruit juices. They consist of water, mixed with concentrate and extra sugar liberally added. Even 100% real fruit juice, still has a high concentration of fructose because so many more fruits are used. A 300ml orange juice by contain 4-5 oranges and have the same sugar content as a fizzy cola drink. There is also little chewing resistance to slow down consumption, making it very easy to consume a large amount of sugar in a short period of time. This lack of pulp significantly speeds up gastric emptying and GI. There is certainly some truth in the commonly used Californian expression “Eat your fruit – Juice your vegetables”
Smoothies; Those where the whole fruit has been put in the blender are better as they maintain the pulp and fibre. They still have a high fructose content especially if sugary fruits such as grapes, pears, apples and mangos are used. To overcome this, the smoothie aficionados often add less sweet fruits such as avocado, vegetables such as kale and spices such as ginger, which lowers the sugar content and enhances the polyphenols content.
Table of percentage sugar levels in common foods
% whole food % whole food
Table sugar 100% Low Fat Granola 28%
Brown sugar 97% Pickled Relish 29%
Fructose syrup 93% Chocolate Ice Cream 25%
Honey 82% Frozen Yogurt 24%
Butterscotch 81% Grapes 16%
Boiled sweets or mints 80% Cherries 14%
Fudge and toffee 80% Bananas 14%
Sucralose (Splenda) Sweetener 80% Apples 13%
High-Fructose Corn-Syrup 76% Pomegranate 10%
Molasses 75% Kiwi 10%
Maple Syrup 72% Pineapple 11%
Dried mango 70% Honey melon 8%
Currents/raisins 65% Figs 7%
Dates 63% Plum 7.5%
Creamed sandwich biscuits 61% Blueberries 7%
Dried papaya 55% Blackberries 6%
Dried pear 55% Strawberries 6%
Dried fig 55% Papaya 6%
Chocolate-Hazelnut Spread, 53% Casaba melon 5.5%
Most Jams 49% Cataloupe melon 5.5%
Frosted corn cereals 39% Tomato 2.5%
Cocoa Crispies 39% Lemon 2.5%
Chocolate Chip Cookies 37% Avocado 0.9%
Cranberry Sauce 37% Lime 0.2%
Other factors which lower GI
As well as the type of carbohydrate, the timing and total content of the entire meal has an influence on GI. Carbohydrates eaten alone will be absorbed quicker but eaten with fat, protein, and fibre slows gastric emptying, which has less of an impact on blood sugar levels. Wholemeal bread has a slower absorption, as well as more vitamins and fibre, than typical thin white bread which to add to the insult, often has table sugar added. Whole meal or fava bean enriched pasta as well as al dente pasta have a slower GI than overcooked white pasta (Tunco). Processed sugars on an empty stomach, such as first thing in the morning, is particularly harmful as they are absorbed rapidly. Conversely, a small sweet dish after a healthy meal will have less of an impact as the stomach has a plenty of other food to slow the gut down. Likewise, as mentioned above, eating the whole fruit will reduce the impact of the sugar in the juice as the pulp and fibre slow gastric emptying.
Polyphenols and their beneficial effect on sugar uptake and diabetes
It has long been know that higher intake of polyphenol rich foods such as turmeric, cinnamon; broccoli, tea, coffee, chocolate, pomegranate, red wine and berries are linked to a lower risk of type two diabetes T2D (Bi, Xiao). The most notable studies included The Nurses’ Health Study, which investigated urinary excretion of eight polyphenol metabolites and found that anthocyanins, flavanones and flavonols as well as the phenolic acid, caffeic acid, were associated with a significantly lower T2D risk (Sun). This was in accordance with the Health Professionals Follow-Up Study, which found that higher polyphenol intake was significantly associated with a lower risk of T2D (Wedick). Both the Women’s Health Study and a large Finnish cohort study reported that apple consumption of ≥1 apple/day showed a lower risk compared with no apple consumption (Song, Knekt). In addition to these large cohort studies, a laboratory study demonstrated that glucose transport in gut cells was inhibited by flavonoid glycosides and non-glycosylated polyphenols such as epigallochatechingallate (EGCG), rich in green tea [Johnston. A study amongst human volunteers both with and without diabetes reported that polyphenols, especially the large polymeric type or condensed tannins found in leguminous foods significantly reduced the glycemic index of simultaneously consumed carbohydrates (Thompson).
The benefits of polyphenols are not just restricted to lowering blood sugar. One of the pathogenic mechanisms that explain the development and progression of micro and macro vascular complications in diabetes is oxidative stress; increased generation of free radicals and an impaired antioxidant defense system in diabetic conditions induces imbalance of the oxidant/antioxidant status (Evans). Inhibition of these oxidative processes by polyphenols with antioxidant properties could prevent the onset and development of long-term diabetic complications (Bucala, Dembinska-Kiec).
The underlying mechanisms of how polyphenols have sugar lowering properties include inhibition of α-amylase and α-glucosidase, inhibition of glucose absorption in the intestine by sodium-dependent glucose transporter 1, stimulate insulin secretion and reduce hepatic glucose output. Polyphenols may also enhance insulin-dependent glucose uptake, activate 5’ adenosine monophosphate-activated protein kinase (Kim, Xiao).
Cancer promoting biochemical mechanisms of refined sugars
High GI foods or meals with a high GL increase the cancer risk via two pathways – directly influencing chemicals which promote cancer development and growth; indirectly by contributing to the development of diseases which then have an influence on cancer.
Indirect mechanisms
Epidemiologic studies have independently linked high GI foods with a significant risk of obesity, diabetes, dental caries and depression, which, in turn, contribute to the risk of subsequent cancer and poorer outcomes after cancer treatments. The mechanisms of how these are linked to cancer are now described:
Obesity: Several well-conducted cohort studies have linked consumption of high sugar diets and drinks with obesity [Te Morenga. Sugary drinks pack on the pounds because energy in liquid form is less satiating (signaling to body to stop eating when you have had enough calories) than when derived from solid foods, resulting in higher consumption than necessary [Di Meglio. Sugary drinks or meals also trigger a damaging yo-yoing effect on blood glucose and insulin levels - The body responds to an initial sugar rush by rapidly increasing insulin levels that triggers metabolism of the excess sugar, into energy storage such as glycogen in the liver. As sugar has only been around in the human diet for the last 150 years, our body thinks that this level of sugar hitting the blood stream must be associated with a very large meal of complex fats and carbohydrate so it over produces insulin which then causes sugar levels to drop (Hypoglycaemia) stimulating hunger, fatigue and lightheadedness. The natural reaction to this is to consume another high calorific sugary snack or drink, which gives instant relief but starts the process all over again. Obesity, especially in postmenopausal women, increases levels of oestrogen, insulin like Growth factor (IGF) and other hormones such as leptin, all of which in laboratory experiments increase proliferation and markers of aggressiveness and spread of cancer cells (Surmacz, Calle). No surprise then that numerous observational studies indicate that weight gain increases cancer risk (Harvie, Eileassen, Teraz, Huang) but also a greater risk of relapse and worse overall survival after successful cancer treatments (Palmqvist, Meyerhardt, Freedland).
Fortunately, it’s never too late to cut out sugar, a meta-analysis of 68 studies showed that individuals who embarked on diet plans which reduced sugar intake instead for more slow release energy sources lead to a significant decrease in body weight (Te Morenga). Loosing weight, fasting and exercise are associated with a lowering of IGF levels and a decreases breast cancer risk [Wu. More specifically, in the Iowa Women’s Health Study, the women who maintained weight loss follow a healthy living programme had a 20–40 % reduction in postmenopausal breast cancer risk compared with women who continued to gain weight [Harvie.
Diabetes and glucose intolerance: Independent from the risk from obesity, high sugar intake directly increases the risk of diabetes by overloading the insulin pathways (Basu). Individuals with T2D have higher serum insulin levels (hyperinsulinemia) as the pancreas produces more and more to try and overcome cellular insulin resistance, considered to be independent risk factors for cancer development, probably related to insulin receptor stimulation on cancer cells (Nicolucci). In addition, hyperglycemia-related oxidative stress and low-grade chronic inflammation, both associated with diabetes, promote malignant transformation (Lorenzi, Richardson). It is not a surprise, therefore, a study involving 872,706 Australians cross referenced the National Diabetes Service Scheme with the National Death Index and found a significant link between type 2 diabetes and fatal colon and pancreatic cancer but also cancers of the liver, uterus, kidney, thyroid, gallbladder and blood (leukaemia) [Harding. Likewise, in the UK, a total of 62,809 patients with diabetes were found to have a higher risk of colon and pancreatic cancer compared to a similar population without diabetes especially if also obese (Curie). Because of these, and many other data, the American Diabetes Association and the American Cancer Society have issued a consensus report stating that 2TDM infers a two fold higher risk for cancers of the liver, pancreas, and endometrium, and a 1.5 fold increased risk for cancers of the colon and rectum, breast, and bladder based (Giovannucci). Even without a formal diagnosis of diabetes, research, funded by the WCRF, found that among half a million people from Norway, Austria, and Sweden, those with an elevated blood glucose (glucose intolerance or pre-diabetes) particularly if overweight were significantly more likely both to develop a range of cancers and to die from it (Stocks).
Depression: An analyses on data from 3486 participants within the Whitehall II prospective cohort reported that those with a high consumption of sugary drinks, sweetened desserts, chocolates, processed meat and fried foods had a 58% increased odds of depression (Akbaraly). Distressing in itself, depression is also linked to increased risk of serious cancer as reported in a study, which followed 41,275 men with prostate cancer from California. They identified 1,894 men with an associated depressive illness and these were 20-80% more likely to die specifically of prostate cancer compared to those with normal mental health [Prasad).
Cholesterol: A study, published in the Journal of the American Medical Association (JAMA), analyzed the dietary habits of a cohort 6110 Americans. After several years, those who eat more than 10% of their daily calories as sugar had raised triglyceride levels and low HDL (good) cholesterol levels [Welsh. Although this lipid pattern is a clear risk for cardiovascular disease it is also known that a higher proportion of LDL (bad cholesterol) compared to the other serum fats is also an increased risk factor for prostate and breast cancer independent of other lifestyle habits (Kitahara).
Dental caries: Sugar consumption is a major cause of tooth decay, especially the consumption of boiled sweets, toffee and sugary drinks (Burt). What is less well known is that dental caries may also be an increased factor for bowel cancer. Two studies, between them looked at more than 100 samples of healthy and cancerous bowel tissue – one from Canada and another from Boston USA and published in the journal Genome. They both found that DNA codes from bacteria, commonly found in dental caries (Fusobacterium) was present in the bowel cancer genes but not normal genes – this raises a strong suspicion that the bacterial DNA traveling through the body interacts with and gets absorbed into gut cells causing them to become cancerous (Kostic).
Direct mechanisms
Inflammation: There are several laboratory studies, which show that high GI foods promote cancer growth directly but the one that was most convincing involved a group of mice with implanted breast cancers. Half were fed sucrose with their usual meal at comparable levels of Western diets and the other half a normal diet. The western diet led to increased tumour growth and metastasis to the lung and liver, when compared with mice fed a non-sugar starch diet (Yang 2015). This effect was ascribed in part to increased expression of inflammatory markers including 12-lipoxygenase (12-LOX) and its arachidonate metabolites (Yang 2015).
Insulin like growth factor (IGF) The section above explained how sugar increases the risk of obesity, which is associated with higher levels of several hormones, which can trigger cancer. Many of these biological changes can also be generated directly, not necessarily with associated obesity (Wolpin). High sugar and insulin levels also lead to direct overproduction of IGF. After binding to its receptor tyrosine kinase, IGF activates several signaling pathways, leading to the inhibition of apoptosis, the promotion of cell growth and angiogenesis (Yu, Frierer). Higher levels of IGF-1 in humans have been reported to be associated with a greater cancer risk (Ryan, Ma). Furthermore, two very large international studies involving people with treated bowel cancer both reported those who eat higher GL diets had higher average IGF levels and an increased relapse rate after primary surgery and chemotherapy (Palmqvist, Meyerhardt).
Genetic damage Studies have found suggested that high sugar levels can result in the formation of oxidative metabolites which increase intracellular free radicals (Bucala). Certainly markers of single strand DNA breaks have been reported in the presence of hyperglycaemia (Lorenzi). Other laboratory experiments using Vitamin B6 deficient flies (more susceptible to genetic damage) reported that feeding them with pure sugar led to significantly higher direct DNA damage and chromosome instability (Marzio).
Clinical evidence of a link between processed sugar intake and cancer risk.
Despite the extent of the direct and indirect mechanisms of ways sugar intake can cause harm, cynics still argue that as there is a lack randomised controlled trials (RCT), the link cannot be substantiated in humans. Although RCT’s are the “gold standard” evidence, not all lifestyle factors can be assessed in this design. It would be near impossible randomise two large groups of individuals, to either eat a high sugar diet or no sugar at all to find out if the cancer risk is different several years later. Likewise, asking people living with cancer to be randomised to a high sugar diet or not to see if it affects the cure rate is unfeasible. In both scenarios, people will simply eat what the want after the first few weeks, making any results meaningless. Despite the deficit in RCT’s there are still an enormous amount of clinical data from large, well conducted environmental and prospective cohort studies measuring their lifestyle habits and recording diseases incidence and outcomes. Examples of the most prominent are summarised here:
* A combined analysis of the Nurses’ Health Study and the Health Professionals Follow-up Study provided data on 100,000 participants for up to 20 years. The 1,809 people who developed colorectal cancer had a history of higher intake of processed carbohydrates, sucrose and fructose compared to people without cancer. The effect of these high GI and GL foods was worse in men who were overweight (Michaud 2005).
* A cohort study from Iowa (USA), evaluated 35,215 women for 10 years. The 212 cases of colon cancer had a higher intake of sucrose-containing foods and beverages other than ice cream/milk products. Again this risk was worse in those with overweight and curiously people who were taller (Bostick).
* A further analysis of the Nurses’ Health Study, identified 180 case of pancreatic cancer. Those particularly women, who were overweight and sedentary with a habit of eating meals with a high GL had a 53% increased cancer risk (Michaud).
* A study from University of Minnesota, looked at the dietary habits of more than 60,000 adults from Singapore for 14 years. They reported that drinking two or more sugary soft drinks a week nearly doubled the risk of developing any cancer and increased risk of pancreatic cancer by 87% (Mueller).
How to reduce sugar intake
The table below provides some tips to how to reduce sugar intake with stopping sweets, mints adding sugar to tea, coffee or cereals highest on the list. Most sugary foods can be easily identified, usually advertises label themselves as “Luxury” or “Treats” or use terms such as “spoil yourself”. Maybe it’s time for governments to step in legislate advertisers to use the truth, although “Treating yourself to fatigue, dental caries, obesity, heart disease, diabetes and cancer” doesn’t have the same ring to it. The sugar tax is a step in the right direction but they should use this money to subsidise healthy drinks and foods. It’s a senseless that on a hot summer’s day, a thirsty customer is offered a sugary drink half the price as water on the shelves and often almost quarter of the price of more tasty sugar free drinks.
Sometimes it’s not so obvious were sugar has been added especially as some of these foods my be advertised as healthy – reduced fat ready meals, salad dressings, pasta sources, yogurt or muesli cereals. It is worth reading the label of processed foods such as “ready meals” or even crisps where sugar is often added to supposedly enhance the flavour. Some restaurants add sugar to their curries and stews – you can instruct the waiter to ask the chef to omit the sugar.
The cancernet.co.uk blog has a series of practical recipes, which maintain a high taste but have no sugar. They also emphasise phytochemical rich foods, which as mentioned above, also reduce the GI or carbohydrates. A number of natural nutritionist update the blog monthly with fresh ideas supported by a short video clip explaining how the dishes are made (cancernetuk).
Diabetic treatments and cancer
Numerous epidemiologic studies and subsequent meta-analyses have repeatedly indicated that T2DM patients receiving metformin, compared to those taking other anti-diabetic medications, have a decreased risk of the occurrence of various types of cancers by 30-50% (Kasznicki, Quinn). Most notably, in the UK, a total of 62,809 patients with diabetes were found to have a higher risk of pancreatic cancer, particularly if also obese, but a lower risk if they were taking metformin monotherapy as opposed to gliclazide or insulin (Curie 2012). This finding was substantiated by a pooled analysis of 108,161 patients with T2DM, which reported that metformin treatment was associated with a significantly lower risk of colorectal cancer [Zhang. Data from 3,837 patients obtained from several databases in Ontario (Canada) noted that the longer duration of metformin treatment after diagnosis of prostate cancer was associated with a significant decrease in all-cause mortality (Margel). In the USA, 68,019 postmenopausal women participating in Women’s Health Initiative clinical trials, women with diabetes had a lower risk of breast cancer if taking metformin [Chlebowski).
One proposed indirect mechanism for metformin’s benefit lies in the fact that it improves cellular sensitivity to insulin and hence reduces IGF in those developing insulin resistance [Yu. Other studies have demonstrated a direct anticancer via inhibition of the mammalian target of rapamycin complex 1 (mTORC1). Metformin is thought to inhibit mTORC1, which plays a pivotal role in metabolism, growth and proliferation of cancer cell [Chiang. Although prospective randomised trials confirming the protective benefits of metformin have not been completed, these data are very convincing, especially as they involved such large numbers and are from independent prestigious organisations. It certainly would be common sense, if diabetic, to ask your doctor to take metformin as opposed to glyclazide if otherwise medical feasible [Margel.
Calorie restriction
A number of studies are now investigating the hypothesis that, if the data shows that overeating is bad, then maybe calorie restriction could be good. Several laboratory experiments have demonstrated that cancer susceptible rats have a lower risk of developing cancer if they had intermittent energy restriction compared to those eating as much as they wish (Harvie 2012). Other animal experiments have reported better response to treatment of fasting before chemotherapy [Meynet.
In humans, a study involving women with breast cancer, has revealed that overnight fasting 13 hours was associated with a statistically significant, 36 percent lower risk of breast cancer recurrence and a non-significant, 21 percent higher probability of death from the disease compared to patients had a short time between the last evening meal and breakfast. The study also reported that fasting more hours per night was associated with significantly better sleep and lower levels of glycated hemoglobin (HbA1c), which is a measure of average blood sugar levels over a period of months. These findings are relevant to cancer prevention and control efforts because elevated HbA1c and poor sleeping habits have been previously been linked to an increased risk of breast cancer. (Marinac). Another small study with female volunteers investigated intermittent energy restriction (IER) in the form of a 2:5 diet (2 days of 65 % energy restriction per week). Researchers reported a 4.8% weight reduction and an 8% reduction in total body fat over one month. Fifty five percent demonstrated increased changes in lipid and glycogen synthesis and reduced markers of insulin resistance. Forty percent had increases in genes changes in breast gene expression associated with breast epithelial cell differentiation (Harvie 2016). Although this remains a subject of interesting future research, the practice of prolonged fasting after cancer raises nutritional concerns should only be undertaken under strict supervision.
In conclusion, although much of the evidence for the cancer-promoting risks of sugar and high GI carbohydrate is from laboratory or large cohort trials, considering all the studies together, the link to cancer is becoming increasingly convincing. People who argue against the risks of sugar should realize that it is not possible to design randomized controlled trials for every lifestyle habit. The logical conclusion, based on existing evidence, is that it is extremely likely that long-term high sugar intake is harmful for many diseases. Instead of the pro-sugar camp claiming that more trials are needed to prove the link, perhaps a more sensible approach is to assume there is a link, unless proven otherwise as certainly no study to date has ever suggested sugar is healthy and the problem is getting worse.
Sugar is widely now available, cheap and its consumption is growing rapidly, especially in low and middle income countries. Between 2000/2001 and 2013/2014 global sugar consumption grew from about 130 to 178 million tonnes, and is expected to reach about 182 million tonnes in 2014/2015. Curbing the sugar growth should be a major priority for governments but as individuals, we can use consumer power by simply not buying sugary foods which will force the food industry to sit up, take note and stop cramming sugar into anything and everything on the supermarket selves.
Summary – tips to reduce sugar and high GI carbs:
Reduce or avoid:
Adding sugar to tea or coffee or to food during cooking
Processed foods, pre-packed ready meals or those labelled as ‘diet’
Sweet snacks: sweets, biscuits and bars
Cakes, sponges and muffins unless they are low sugar
If you do eat cakes cut off the icing and sugary toppings
Sweet drinks such as cola or other fizzy drinks
Restaurants which add sugar to their meals
Processes fruit juices with the pulp removed
Sugary breakfast cereals especially with added sugar or honey
Change from white to wholemeal bread
Don’t eat white toast and jam for breakfast
Use wild rice instead of white rice
Eat salad and vegetables with white pasta to slow its GI
Try quinoa instead of white rice or pasta
Alternatively:
For a treat consider chocolate made without sugar
Make cakes without sugar - use fruits such as dates or banana instead.
If you need to add something sweet – natural alternatives eg Stevia
For snacks, consider sticks of crunchy vegetables or nuts
If you are craving something sweet – restrict to post meal times
For a snack easy-to-eat fruit such as grapes, nuts, bananas and satsumas
Eat the whole fruit
Drink blended fruit and vegetable smoothies rather than juices
Drink water or iced tea
References
Akbaraly T, Brunner E, Ferrie J et al. Dietary pattern and depressive symptoms in middle age. The British Journal of Psychiatry 2009, 195
(5) 408-413.
Basu S, Yoffe P, Hills N et al. The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data Plos 2013. DOI: 10.1371/journal.pone.0057873
Bi X, Lim J, Chritiani J et al Spices in the management of diabetes. Food Chemistry. 2017 Vol 217; pp281-293.
Bostick R, Potter J, Sellers T et al Sugar, meat, and fat intake, and non-dietary risk factors for colon cancer incidence in Iowa women Cancer Causes & Control 1994, 5 (1), pp38-52.
Bremer A, Kimber S, Graham J et al Fructose-fed rhesus monkeys: A nonhuman primate model of insulin resistance, metabolic syndrome, and type 2 diabetes. Clin Transl Sci. 2011; 4(4): 243-252.
Bucala R, Armitage P & Doll R et al. Modification of DNA by reducing sugars: a possible mechanism of nucleic acid aging, age-related dysfunction in gene expression. 1984, Proc Natl Acad Sci USA 81;105-109.
Burt BA and Pai S. Sugar consumption and caries risk: a systematic review. J Dent Educ 2001; 65: 1017-23.
Calle EE and Kaaks R. Obesity, hormones and cancer; epidemiological evidence and proposed mechanism. Nature Reviews Cancer 2004, 4, 579-591.
Chiang GG, Abraham RT.. Targeting the mTOR signaling network in cancer. Trends Mol Med 2007;13:433-42.
Chlebowski RT, McTiernan A, Wactawski-Wende J, et al. Diabetes, Metformin, and Breast Cancer in Postmenopausal Women. J Clin Oncol 2012;30:2844-52.
Currie C, Poole C and Gale E et al. The influence of glucose-lowering therapies on cancer risk in type 2 diabetes Diabetologia 2009, 52, (9) 17-66-77.
Currie CJ, Poole CD, Jenkins-Jones S et al Mortality after incident cancer in people with and without type 2 diabetes: impact of metformin on survival. Diabetes Care. 2012; 35(2):299-304.
DiMeglio DP, Mattes RD. Liquid versus solid carbohydrate: effects on food intake and body weight. Int J Obes Relat Metab Disord 2000;24:794-800.
Dembinska-Kiec A, Mykkänen O, Kiec-Wilk B et al . Antioxidant phytochemicals against type 2 diabetes. Br J Nutr. 2008;99:es109–ES117.
Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. Endocr Rev. 2002;23:599–622.
Eliassen AH, Colditz GA, Rosner B, Willett WC, Hankinson SE. Adult weight change and risk of postmenopausal breast cancer. JAMA. 2006;296(2):193–201.
Freedland SJ, Aronson WJ, Kane CJ et al Impact of obesity on biochemical control after radical prostatectomy for clinically localised prostate cancer:. JCO 2011; 22(3) 446-53
Freier S, Weiss O, Eran M, et al.; Expression of the insulin-like growth factors and their receptors in adenocarcinoma of the colon. Gut 1999; 44: 704-708.
Giovannucci E, Harlan E, Archer E et al. Diabetes and cancer: a consensus report. Diabetes Care 2010: 33(7): 1674-85.
Harding J, Shaw J, Peeters A et al Age-Specific Trends From 2000-2011 in All-Cause and Cause-Specific Mortality in Type 1 and Type 2 Diabetes: A Cohort Study of More Than One Million People. Diabetes Care. 2016: 39(6): 1018-26.
Harvie M, Howell A. Energy restriction and the prevention of breast cancer. Proc Nutr Soc. 2012;71(2):263–75.
Harvie M, Sims A, Pegington M et al. Intermittent energy restriction induces changes in breast gene expression and systemic metabolism 2016 Breast Cancer Research 18:57
Harvie M, Howell A, Vierkant RA, et al. Association of gain and loss of weight before and after menopause with risk of postmenopausal breast cancer in the Iowa women’s health study. Cancer Epidemiol Biomarkers Prev. 2005;14(3):656–61.
Huang Z, Hankinson SE, Colditz GA, Stampfer MJ, Hunter DJ, Manson JE, et al. Dual effects of weight and weight gain on breast cancer risk. JAMA. 1997;278(17):1407–11.
Johnson R, Segal MS, Sautin Y, et al. Potential role of sugar (fructose) in the epidemic of diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007;86:899-906.
Johnston K, Sharp P, Clifford M Dietary polyphenols decrease glucose uptake by human intestinal Caco-2 cells FEBS letters 2005; 576 (7), pp 1653-1657
Johnson R, Perez-Pozo SE, Sautin YY et al. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes? Endocr Rev 2009;30:96-116.
Kasznicki J, Sliwininska A and Drzewoski J. Metformin in cancer prevention and therapy. Ann Trasl Med. 2014;2(6):57-61
Knekt P, Kumpulainen J, Jarvinen R, et al. Flavonoid intake and risk of chronic diseases. Am. J. Clin. Nutr. 2002;76:560–568
Kim Y, Keogh L, Clifton P. Polyphenols and glycemic control. Nutrients 2016 5;8(1).
Kitahara C, de González B, Jee S et al Total Cholesterol and Cancer Risk in a Large Prospective Study. 2011 J Clin Oncol 29:1592-98.
Kostic A, Ojesina A, Pedamallu C et al. Genomic analysis identifies association of Fusobacterium with colorectal carcinoma18, 2011, doi: 10.1101/gr.126573.111
Te Morenga L, Mallard S, Jim Mann J et al Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies BMJ 2013;346:e7492
Livesey G and Taylor R. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies; but reports on isocaloric comparisons. Am J Clin Nutr2008;88:1419-37.
Lorenzi M, Montisano DF, Toledo S et al. High glucose induces DNA damage in cultured human endothelial cells. 1986. L clin Invest 77(1) 322-25.
Margel D, Urbach DR, Lipscombe LL, et al. Metformin use and all-cause and prostate cancer-specific mortality among men with diabetes. J Clin Oncol 2013;31:3069-75.
Marinac CR, Nelson SH, Breen CI, Hartman SJ, Natarajan L, Pierce JP, Flatt SW, Sears DD, Patterson RE. Prolonged Nightly Fasting and Breast Cancer Prognosis. JAMA Oncol. 2016;2(8):1049-1055.
Marzio A, Merigliano C, Gatti M et al. Sugar and Chromosome Stability: Clastogenic Effects of Sugars in Vitamin B6-Deficient Cells PLoS Genet. 2014; 10(3): e1004199.
Meyerhardt JA, Sato K, Niedzwiecki D. Dietary glycemic load and cancer recurrence and survival in patients with stage III colon cancer: findings from CALGB 89803. J Natl Cancer Inst. 2012 21;104(22):1702-11.
Michaud D, Fuchs C, Liu S et al. Sugar, and Colorectal Cancer Risk in Men and Women
Cancer Epidemiol Biomarkers Prev January 2005 14; 138.
Michaud D and Liu et al Dietary Sugar, Glycemic Load, and Pancreatic Cancer Risk in a Prospective Study JNCI J Natl Cancer Inst (2002) 94 (17): 1293-1300.
Mueller N, Odegaard A, Anderson K et al Soft drink and juice consumption and risk of pancreatic cancer: the Singapore Chinese Health Study. Cancer Epidemiol Biomarkers Prev. 2010; 19(2):447-55.
Ma J, Pollak M, Giovannucci E et al. Prospective study of colorectal cancer risk in men and plasma levels of Insulin like growth factor (IGF)-1 and IGF binding protein-3. J Natl Cancer Inst. 1999 7; 91 (7): 620-5.
Nicolucci A. Epidemiological and biochemical aspects of neoplasms in diabetes. Acta Diabetol 2010; 47: 87–95
Palmqvist R, Halmans G, Rinaldi S, et al. Plasma insulin-like growth factor, insulin-like growth factor binding protein, and colorectal cancer: a prospective study in Sweden. Gut 2002; 50: 642-6.
Prasad S, Gu X, Lipsitz SR, et al Effect of Depression on Diagnosis, Treatment, and Mortality of Men With Clinically Localized Prostate Cancer. JCO, 2014 JCO.2013.51.1048
Richardson LC and Pollack LA. Therapy insight: influence of type 2 diabetes on the development and outcomes of cancer. Nat Clin Pract Oncol 2005; 2:48-53
Ryan CJ, Hagg CM, Simko J, Nonaka DF, Chan JM, Weinberg V, et al. Expression of insulin-like growth factor-1 receptor in local and metastatic prostate cancer. Urol Oncol 2007;25:134 – 40.
Silbernagel G, Machann J, Unmuth S et al. Effects of 4-week very-high-fructose/glucose diets on insulin sensitivity, visceral fat and intrahepatic lipids: an exploratory trial. Br J Nutr. 2011;106:79-86
Song Y, Manson J, Buring J, et al. Associations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women: A prospective study and cross-sectional analysis. J. Am. Coll. Nutr. 2005;24:376–384.
Stocks T, Rapp K, Bjørge T, et al Blood Glucose and Risk of Incident and Fatal Cancer in the Metabolic Syndrome and Cancer Project (Me-Can): Analysis of Six Prospective Cohorts. Plos 2010 DOI: 10.1371/journal.pmed.1000201
Sun Q, Wedick N, Tworoger S. et al Urinary excretion of select dietary polyphenol metabolites is associated with a lower risk of type 2 diabetes in proximate but not remote follow-up in a prospective investigation in 2 cohorts of US women. J. Nutr. 2015 doi: 10.3945/jn.114.208736.
Surmacz E. Obesity hormone leptin; a new target for breast cancer? Breast Cancer Res 2007; 9(1): 301.
Thompson L, Yoon I, Jenkins D et al Relationship between polyphenol intake and blood glucose response of normal and diabetic individuals. Am J Clin Nutr 1984
vol. 39
(5) 745-751Teras LR, Goodman M, Patel AV, Diver WR, Flanders WD, Feigelson HS. Weight loss and postmenopausal breast cancer in a prospective cohort of overweight and obese US women. Cancer Causes Control. 2011;22(4):573–9
Tunco I, Bacchotti T, Barden C. Polyphenol content of Fava bean enriched pasta reduced GI post ingestion. Functional Foods in Health and Disease. 2016; 6)5) 291-305
Wedick N, Pan A, Cassidy A, et al. Dietary flavonoid intakes and risk of type 2 diabetes in US men and women. Am. J. Clin. Nutr. 2012;95:925–933.
Welsh J, Sharma A, Abramson J et al Caloric sweetener consumption and dyslipidemia among US adults.2010 JAMA 21; 303(15),1490-7.
Xiao J and Hoegger P. Dietary polyphenols and type 2 diabtes: current insights and future perspectives. Curr Med Chem. 2015(1):23-8.
Yang J Chan D, Felix E et al A Sucrose-Enriched Diet Promotes Tumorigenesis in Mammary Gland in Part through the 12-Lipoxygenase (inflammatory) pathway. 2015 Cancer Res; 76(1); 24–29.
Yu H, Rohan T. Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst 2000; 92: 1472–89.
Wedick N, Pan A, Cassidy A, et al. Dietary flavonoid intakes and risk of type 2 diabetes in US men and women. Am. J. Clin. Nutr. 2012;95:925–933.
World Cancer Research Fund International. ‘Curbing global sugar consumption: Effective food policy actions to help promote healthy diets and tackle obesity’, 2015
WHO / Food and Agricultural Organization joint report. Carbohydrates in human nutrition. FAO Food Nutr Pap 1998; 66:1-140.
Zhang ZJ, Zheng Z, Kan H, et al. Reduced Risk of Colorectal Cancer With Metformin Therapy in Patients With T2DM. A meta-analysis. Diabetes Care 2011;34:2323-8.
Author's Note:
Professor Robert Thomas. Consultant Oncologist, Bedford & Addenbrooke’s Hospitals, Cambridge University NHS Trust, Professor of Biological and exercise Science Coventry University. c/o The Department of Oncology, Box 193, Addenbrooke’s Hospital, Cambridge CB2 2QQ [
[email protected].
Kristina Kis. Exercise and nutritional advice practitioner The Greenery Health Zone, 18 Sylvan Av, London NW7 2JJ [
[email protected]
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