22.04.2014 Natural Health

Not So Sweet

Just one can of soft drink a day increases the risk of heart attack - and the more sugar we consume the greater the health risk, says Peter Dingle PhD

Just one can of soft drink or the equivalent in sugar or sugary food produces immediate toxic effects on the body and contributes to major chronic illnesses 20-30 years down the line. It is equivalent to smoking half a pack of cigarettes a day. The major areas of health concern with high sugar consumption include certain cancers, cardiovascular disease such as stroke, heart attack, obesity and type 2 diabetes, dental caries, bone fractures and osteoporosis, kidney stones and more.

While the particular dynamics of the illnesses may be different to cigarette consumption, the long term health costs to individuals and the economy are much the same. However, because of space limitations I have just focused here on sugar and cardiovascular disease - the number one killer in Australia.

An overwhelming body of evidence points to the detrimental role of sugar - mostly sucrose (table sugar) and high fructose corn syrup - along with other refined carbohydrates in weight gain and the development of diabetes and all forms of cardiovascular disease and cancer. Knowledge of the link between cardiovascular disease and sugar consumption dates from the 1960s and 1970s, when Yudkin and colleagues discovered an association between increased sugar consumption and increased cardiovascular disease incidence in both national and international comparisons (1).

Astonishingly, no clear threshold exists for the multitude of adverse effects of sugar intake; in general the association seems to be roughly linear, which means the more you take in, the more harm it does to your body and mind. Diets high in added sugar raise heart disease risk: just one soft drink a day raises heart attack risk. A major analysis by the Centers for Disease Control and Prevention (CDC) found that most adults in the US consumed 10% or more of calories from added sugar (71.4%); approximately 10% consumed 25% or more. Participants who consumed 10% to 25% had a 30% increased risk of cardiovascular disease, while those consuming 25% or more calories from added sugar increased their risk of CVD mortality by 275% (2).

A five year study of males aged 40 to 64 years found that chronic heart disease mortality rate doubled in individuals with high blood sugar; the increase was independent of age and blood pressure (3). Results from the Nurses' Health Study found that women whose diets consisted of a high glycaemic load (high blood glucose from sweets or highly processed starch) had an increased chronic heart disease risk, with those in the highest consumption group showing a two fold increase in CHD risk throughout the 10 year follow-up (4).

Similarly, a prospective cohort study of more than 40,000 men found that consuming sugar-sweetened drinks is associated with an increased risk of coronary heart disease (5). Increasing scientific evidence shows a link between sugar and increasing blood pressure (6,7,8). The Framingham Study reported that consumption of more than one soft drink per day significantly increases one's risk of developing high blood pressure and metabolic syndrome, regardless of whether it is a diet or regular beverage (6,7).

Risks Showing up in Childhood

In a study of 4,867 adolescents aged 12 to 18 years, blood pressure increased as did serum uric acid, which is linked to gout and some forms of arthritis, by 0.18 mg/dL with sugar-sweetened beverage consumption (9). In a study of 2,388 school children aged nine to 12 years, plasma sugar concentrations were found to be positively correlated with blood pressure, independent of weight (10). Of great concern is that these findings suggest that the relationships between risk factors for coronary heart disease that exist in adults are already evident in childhood (11).

The consumption of sugar-sweetened beverages (SSBs) has been associated with an increased risk of type 2 diabetes and coronary artery disease (12,13). Based on data from 310,819 participants, individuals in the highest levels of sugar-sweetened beverage intake (most often one to two servings per day) had a 26% greater risk of developing type 2 diabetes than those in the lowest level. In addition to weight gain, higher consumption of SSBs is associated with development of metabolic syndrome (14). An excess of fat in the liver, called fatty liver disease, is a response to dietary sugar and is one of the main causes of metabolic syndrome (15,16). In one study, a seven day high-fructose diet increased lipid deposition in liver and muscle and fasting VLDL-triacylglycerols and decreased hepatic insulin sensitivity (17).

It has been known for some time that carbohydrates can increase the risk of cardiovascular disease by altering lipid profiles. All carbohydrates are broken down into monosaccharide form prior to absorption by the body; these monosaccharides enter the liver and undergo glycolosis before being released into the bloodstream as glucose (18,19). This process in turn triggers the release of insulin from the pancreas to drop blood sugar levels (20). The release of insulin from the beta cells within the pancreas (21) ensures the regulation of blood sugar levels via positive and negative closed feedback loops according to the level of sugar within the bloodstream (22). Apart from regulating blood sugar concentrations, insulin serves to inhibit the breakdown of fat within adipose tissue by limiting the effectiveness of the hydolysation of triglycerides to release fatty acid; thus leading to heightened risks of cardiovascular disease (23,24).

Risks even in low sugar doses

Even low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation oxidation, even in young healthy individuals (25). High fructose corn syrup (which replaces cane sugar in the US) was seen to bring on an inflammatory response within rat kidneys (26), showing that the dietary intake of fructose, in the same concentrations as other dietary sugars such as starch or glucose, was more likely to induce certain features indicative of metabolic syndrome in humans as well as in rodents.

The results of these studies demonstrate that increased added sugars are associated with important cardiovascular disease risk factors, including lower HDL-C levels, higher triglyceride levels, and higher ratios of triglycerides to HDL-C. Elevations in fasting plasma triglycerides, principally very-low-density lipoproteins, are a consistent feature of diets high (>20% of energy) in sucrose, glucose, and fructose (27). About 85% of the body's cholesterol is manufactured in cells, mostly in liver and in intestinal mucosa, with only about 15% the dietary input. The manufactured lipids leave the liver in the form of VLDL. Large amounts of sugars in one's diet result in elevation of triactlglycerol concentration and LDL cholesterol and a depression of HDL cholesterol; this reflects hepatic secretion of VLDL and impaired clearance (28,29). In addition, glucose in blood adversely affects cholesterol stabilising capacity (30).

A study of 6,000 adults (31) found a high intake of added sugar is associated with increased risk for low HDL cholesterol and high triglycerides (blood fats). Compared with adults who got less than five percent of their total energy intake from added sugars, those getting 17.5% to 25% of their energy from added sugars were about twice as likely to have low HDL levels. Another study found a statistically significant correlation between dietary added sugars and blood lipid levels in adults. A similar case study examining the effects of two varying diets on the degree of LDL trigycerol levels within humans concluded that a high fructose diet over a period of four weeks that exceeded the recommended daily energy requirements of the test subjects by 16% caused a sustained increase in the LDL cholesterol levels within the bloodstream (32), thus increasing the risk of cardiovascular diseases.

A study on the difference in effects of glucose and fructose-sweetened drinks on individuals of the same body mass index, over a period of 10 weeks, concluded that both groups had put on weight over the test period (33). It was, however, noted that the group that had consumed the fructose-sweetened drinks with every meal had a much higher percentage of visceral fat that is known to be more adhesive to the linings of organs, as well as higher levels of LDL cholesterol, thus increasing the risk and likelihood of arthrosclerosis and cardiovascular diseases.

The overwhelming evidence shows sugar consumption increases weight gain; studies during which people have reduced sugar and processed carbohydrate consumption have consistently seen people lose weight. A meta analysis of prospective studies and randomized trials that examined freely consumed sugar highlighted the adverse effect of sugar on body weight in adults (34,35). This evidence includes two recent randomised trials in children (36,37).

Impact on Brain Health

Sugar has a serious effect on our brain health. When you eat carbohydrates, which break down into sugar in the body, your blood sugar levels become elevated. High blood sugar levels also create inflammation, contributing further to damage in the brain and, over time, a diet high in sugar leads to an accelerated death of healthy brain cells. The brain cells shrink and become tangled, increasing the likelihood of developing lesions in the brain, which are linked to Alzheimer's. In a study of 2,067 participants without dementia, researchers found higher glucose levels were a risk factor for dementia, even among persons without diabetes (38).

Another recent study reported that improved blood sugar control and better brain function were found in non-diabetics. This presents the possibility that scaling back on blood sugar-disruptive carbohydrates, such as those rich in sugar and starch, could well be a good tactic for those of us wishing to preserve mental functioning as we age, whether we have diabetes or not (39,40).

Even short-term exposure to sugary or junk food diets damages the brain and impacts memory. In two experiments on rats to examine the effects of short-term exposure to a diet rich in sugar and fat or rich in sugar, rats fed a cafeteria-style diet containing chow supplemented with lard, cakes, biscuits and a 10% sucrose solution performed worse on the place recognition, but not the object recognition task, than chow-fed control rats when tested after five, 11, and 20 days.

In a subsequent experiment, rats fed the cafeteria-style diet either with or without sucrose, along with rats fed chow supplemented with sucrose also performed worse on the place, but not the object recognition task when tested. Rats fed the cafeteria diets consumed five times more energy than control rats and exhibited increased plasma leptin, insulin and triglyceride concentrations; these were not affected in the sucrose-only rats. Rats exposed to sucrose exhibited both increased hippocampal inflammation and oxidative stress. In contrast, these markers were not significantly elevated in rats that received the cafeteria diet without added sucrose.

These results show that relatively short exposures to diets rich in both fat and sugar, or rich in sugar alone, impair hippocampal-dependent place recognition memory prior to the emergence of weight differences, and suggest a role for oxidative stress and neuroinflammation in this impairment.

No matter how one looks at it, soft drinks, whether "diet" or not and sugary foods are not suitable for human consumption.

DISCLAIMER: Dr Peter Dingle is a researcher, educator and public health advocate. He has a PhD in the field of environmental toxicology and is not a medical doctor.

References

Howard and Rosett 2002JAMA Internal Medicine, February 3, 2014;Fuller et al. 1979Howard and Rosett 2002De Koning et al. Circulation 2012; 125:1735-41Appel et al. 2009;D'Agostino et al. 2007;Flicklinger et al. 2010J Pediatr. 2009 Jun; 154(6):807-13. http://www.ncbi.nlm.nih.gov/pubmedFlorey et al. 1976Circulation. 2011; 123(3):249-257Malik et al. Diabetes Care 2010; 33:2477-83;Fung et al. Am J Clin Nutr 2009; 89:1037-42Diabetes Care, November 2010, vol. 33Lutsey et al. Circulation 2008; 117:754-61;Johnson et al. Circulation 2009; 120:1011-20American Journal of Clinical Nutrition 2008, Lê et al.Andrews 2009;David and Ludwig 2002Shaham et al. 2008Saltiel and Kahn 2001Steil et al. 2003Glushakova et al. 2008;Lustig, Schmidt and Brindis. Nature 2012; 482:27-9)Am J Clin Nutr. 2011; 94(2):479-485,Nakagawa HYPERLINK "http://et.al/"et al. 2006Welsh et al. JAMA2010; 303:1490-7Seelay et al. 2000;Frayn and Kingman 1995Wilkens and Krut 1965Welsh et al. 2010 JAMA. 2010; 303 (15): 1490-1497Lê et al. 2006White 2009Te Morenga et al. BMJ 2012; 345:e7492;Malik and Hu, Am J Clin Nutr2011;94:1161-2Ebbeling et al. N Engl J Med 2012; 367:1407-16;De Ruyter et al. N Engl J Med 2012; 367:1397-406Paul K. et al. N Engl J Med 2013Kerti et al. Neurology, 23 October 2013;Seneff et al. Eur J Int Med 2011; 22:134-140
Peter Dingle

Dr Peter Dingle (PhD) has spent the past 30 years as a researcher, educator, author and advocate for a common sense approach to health and wellbeing. He has a PhD in the field of environmental toxicology and is not a medical doctor. He is Australia’s leading motivational health speaker and has 14 books in publication.

http://www.drdingle.com/

https://www.facebook.com/DrPeterDingle/

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