Reviewing Role of Dietary Sugars in Blood Pressure Regulation: Sugar-Induced BP Elevation.
Dietary Sugars, Hypertension
Insulin Resistance, Elevated Blood Pressure
* Elevated blood pressure (BP), a serious health disorder worldwide, is occurring far too frequently.
* Ubiquitous studies concerning cardiac dynamics suggest a major participation of lifestyle, particularly dietary indiscretions, in the frequency of raised BP.
* By the end of the 1960's, only table salt (NaCl) among dietary ingredients was clearly associated, to any great extent, with BP elevations--not table sugars (sucrose, fructose, high fructose corn syrup). At the beginning of the 1980s, research began to draw a significant link between challenges with dietary sugars alone and higher BP.
* In addition to salt and water retention, the harmful effects from sugars appear to depend primarily upon development of insulin resistance. In support, a significant correlation between fasting circulating glucose and insulin concentrations with BP has been reported in clinical investigations.
* An interplay between popular dietary sugars and table salt on BP regulation has come to light and should be wisely considered when undertaking the prevention and treatment of the global crisis arising from elevated BP levels.
A major health consideration present nowadays is whether typical amounts of dietary sugars and refined carbohydrates in the modern Western diet can be responsible, at least in part, for the recent global epidemic of elevated BP. (1,2) To simplify the examination of this matter, table sugars will be the primary focus in this review with the knowledge that other refined carbohydrates such as white flour can also similarly influence optimal pressure regulation. Concerning the existence of sugar-induced hypertension, current evidence strengthens and expands the beliefs proposed in earlier reviews. (3,4)
It is only recently that real attention has been given by clinicians and the public to the potential harm to cardiovascular and metabolic health from glucoseinsulin perturbations and higher BP readings secondary to excess table sugar consumption. (5-10) Suffice it to say, blood pressure (BP) regulation within a tolerable range, not too low, nor too high, is very essential in order to achieve a, lasting, healthy existence. (11-13) It is further recognized that maintenance in the lower part of the accepted "normal range" without the development of hypotension is preferred. (2) Despite this generally accepted knowledge regarding benefits behind preserving pressure measurements within an ideal range, high readings continue to provide a serious, ongoing dilemma for the general public. (14-18)
The initial lack of interest in sugar-induced BP elevations in the recent past may have developed, to some extent, from at least two possibilities. First, universal awareness concerning possible damage produced by saturated fat intake on the cardiovascular system directed attention from the harm caused by simple refined carbohydrates like sugars. Recognizing the current beliefs by numerous nutritionists that sugars and other refined carbohydrates are significant dietary offenders in the pursuit for optimal health, (19-22) it is ironic that the initial recommendations to evade saturated fats no doubt led to amplified use of refined carbohydrates like sugars to substitute for the lower intake of calories from saturated fats. (23) As a second reason, much of the early data on the subject of sugar-induced cardiovascular maladies, particularly high BP, was obtained from animal studies. (3,4) Regrettably, results from such laboratory studies were and still are largely overlooked by most practitioners.
In 1982, a review article (4) examined the actuality of sugar-induced BP elevations by assessing information gained primarily from prior laboratory findings. (24) From those previous observations, it was shown that adding sucrose to drinking water free of added sodium in three sub strains of rats (normotensive and hypertensive) caused marked and statistically significant increases in systolic BP. (24) An important observation in these animal studies was that sugar-induced metabolic malfunctions usually occur despite virtually no significant weight gains by the rodents. This confirms current thinking that direct effects of sugars on BP exist, not only secondary events associated with body fat accumulation from surplus caloric intake. (1-2)
Carbohydrate Intake Over the Preceding Century and Beyond
In 1986, Karanja and McCarron published a figure depicting carbohydrate intake in the American food supply. The figure showed that between the years 1909 to 1960 a significant decrease in total carbohydrate consumption had taken place. (25) This decline occurred mainly through a reduced consumption of complex carbohydrates such a whole grains. However, a simultaneous increase in simple carbohydrate consumption had also taken place. In another report, consumption of total carbohydrates steadily increased starting around 1963 despite the fact that fiber consumption remained low. (26) In contrast to fiber, a continuing rise in sugar consumption took place from 1983 to 1999, i.e., 122 pounds per person in 1963 to 158 pounds per person in 1999. (27) This represented a 30% increase.
Presently, the unfortunate trend is to ingest more sugar while consuming low amounts of fibers remains. Certainly, drinking sugar-containing sodas are an excellent example of such. This combination (high sugar, low fiber) has been shown in animal studies to greatly increase systolic BR (4-24) Although many factors are involved in the regulation of BP, the augmented prevalence of hypertension in modern time may be caused, at least in part, by a greater upsurge in consumption of sugars especially from sucrose and high fructose corn syrup. (28,29)
Overall Knowledge Concerning Elevated BP and Its Relationship to Various Cultures
Both the American Heart and American Stroke Associations estimate that the incidence of hypertension will increase 7.2% by 2030 from recent approximations . For example, there were roughly 972 million people living with hypertension worldwide as of the year 2000. Unfortunately, it is estimated that this figure will rise to 1.56 billion by the year 2025. (31) Different ethnic groups are reported to have the following ratios of hypertensive individuals: for non-Hispanic whites 33.4% of men and 30.7% of women; for non Hispanic blacks 42.6% of men and 47.0% of women; and for Mexican-Americans 30.1% of men and 28.8% of women. (32) Despite this growing percentage of the population, a sensible estimation of those currently being treated is that only 50% are under satisfactory pressure control. (33,34)
Some primitive societies also referred to as non-Western in contrast to the modern, Western world show either no change or only a modest decline in BP throughout aging. (35-36) However, high BP not-infrequently appears if individuals from these primitive groups begin to acquire a lifestyle similar to the more modern Western world. Interestingly, movement of individuals from under developed areas to more contemporary settings often causes progressive elevations of BP -suggesting that more factors than just genetic ones are implicated. (35,36) Concerning primitive versus modern lifestyle, an obvious probability behind the pressure differences includes dissimilar dietary backgrounds. More and more individuals are consuming the modern Western diets and more often than not ingest excess calories leading to overweight, eat an improper balance of macronutrients like sugars, fibers, and fats; and consume too much sodium and alcohol and too little potassium. (13,18,37,38)
Harm Linked to Dietary Sugars with Emphasis on the "Yudkin Era"
Regarding the existence of sugar-induced BP elevation among the masses, the early years of the 20th century were extremely important toward the comprehension of its existence. (3) During World War 1, the incidence of diabetes, obesity, and cardiovascular diseases and elevated BP conspicuously fell in every country where the accessible supply of food was absent because of shortages brought on by the war. With these data in hand, Paton (39) suggested that the incidence of obesity, diabetes, and arteriosclerosis regressed primarily from the shortage of dietary sugar. If true, this could explain another happening, i.e., the pathophysiology behind the augmented occurrence of these chronic maladies before the war when a marked boost in sugar consumption had occurred.
In contrast, Aschoff favored another hypothesis. (40) He believed that decreased fat intake rather than decreased sugar intake during the war was the primary reason for the lessening of many metabolic disturbances. Himsworth also noted a lower incidence of diabetes mellitus among the general population during World War I and associated it with the low fat diets common to that time period. (41) Yudkin pointed out a concern when it came to interpretations--lower intakes of both sugars and fats were closely and positively correlated with each other during the First World War. (42) Accordingly, the principal reason for the better health remained in doubt. More information from the Second World War also failed to definitively determine whether dietary sugars or fats were the more important cause of atherosclerotic heart disease and diabetes mellitus; because again, both low sugar and fat consumption took place simultaneously in the face of a falling occurrence of these chronic maladies. (3)
Following World War 2, a series of papers by John Yudkin continued to defend the prospect that overconsumption of sugar and even other refined carbohydrates like white flour were largely responsible for the increasing incidence of diabetes mellitus (type 2) and coronary heart disease. (43,45) To strengthen his assertions, he pointed out that higher intake of sucrose not only raises BP but circulating triglycerides and insulin levels as well. Based on his findings, Yudkin supported a low carbohydrate diet for optimal health, a belief favored later by Atkins et al. in their ketogenic diets. (46)
Even as Yudkin received modest support for his theory based on sugar consumption, the presumption that fats, particularly saturated fats, are even more responsible for the increasing prevalence of cardiovascular diseases received considerably greater backing for many years from both the academic world and the general public. (47,48) Despite much resistance, Yudkin continued to promote sucrose over fats as the major nutritional igniter of many chronic disorders, principally cardiovascular disorders and diabetes mellitus. In the 1970s and 1980s, Yudkin noted that several factors were behind the development of elevated BP and ischemic heart disease, e.g., smoking, physical inactivity, stress, and diet. (42-43) "We cannot therefore expect that any one isolated factor will show an exact association with the disease," since so many biological variations could be involved. Yudkin was adamant in his belief that excess sucrose ingestion elevates circulating triglycerides and insulin and results in a diminished glucose tolerance in man and rodents. (42-45) In truth, diabetes and cardiovascular disorders like hypertension appeared to increase despite attempts to limit saturated fat intake. Suffice it to say, the belief behind the cholesterol theory may have been based largely on imperfect information. (49,50)
Basics Concerning Carbohydrates and Their Metabolism General Background
When elevated BP is present along with overweight/obesity, it seems sensible to diminish caloric intake in order to improve insulin sensitivity. Many associate insulin resistance with pressure elevations. (51-55) Excess caloric intake from fats and sugars may result in unwanted fat accumulation, especially in the liver, that is strongly linked to insulin resistance. (56) In addition, many have contended that "special calories" exist from refined carbohydrates like sugars that particularly need to be avoided for reasons other than increasing the caloric load. (57) What is behind this? The answer is that sugars and numerous refined carbohydrates can worsen the status of insulin sensitivity directly. (57-58) To strengthen this concept, adding excess sugars to the diet consistently enhances insulin resistance and the accompanying systolic BP in rats without elevating body weight. (24,59) Accordingly, lowering calories to reduce body fat is important, but that some carbohydrates through direct actions not necessarily related to accumulation of fat mass still raise BP significantly.
Yudkin in the Journal of the Royal Society of Medicine wrote clearly in 1968 his logic behind the dissimilar responses between sucrose and many of starches: "Present evidence suggests that most of the effects of sucrose are due in small part to its ease of digestion and absorption compared with starch, also in small part to its being a disaccharide, but chiefly to the fructose released when sucrose is digested." (60) Yudkin over 30 years ago proposed two important causes behind sugar-induced pressure elevations favored by many even today. Harm from caloric sweeteners such as sucrose and HFCS lies both in their high glycemic indices (rapid absorption) and the presence of fructose. (61,62)
Focus on Absorption: Glycemic Index and Load
The absorption of carbohydrates in general takes place at different rates--some faster (high glycemic index) than others (low glycemic index). (63,64) This is an important principal, because the absorption rate along with the quantity taken in (glycemic load) can affect the insulin system to a great extent--rapidly absorbed carbohydrates consumed in enough magnitude (high glycemic load) are associated with insulin resistance and many accompanying chronic health maladies such as elevated BP. (60,61)
Viscous fiber can slow absorption of sugars. (64) So, it is unfortunate that the typical modern diet is high in rapidly absorbable sugars--yet, low in fibers. Drugs such as acarbose and natural supplements like l-arabinose impede the activity of alpha-glucosidases such as sucrase and slow absorption. (1,2,65) Additionally, bean and hibiscus extracts can effectively lessen carbohydrates absorption by lowering alpha-amylase activity. Thus, there are a number of means to slow and/or lessen absorption of carbohydrates that, in turn, could improve pressure readings. (65)
Among popular dietary sweeteners, fructose has been perceived to be particularly harmful. In our early studies on sugar-induced BP elevation carried out in the late 70's, fructose, on a weight basis, had the greatest influence on BP--more so than glucose or sucrose. (24) In any case, it would appear to be prudent to limit the daily consumption of common dietary sources of fructose such as sucrose and HFCS.
Over a recent span of years, numerous findings suggest that fructose consumption regularly has the capability to present deleterious health problems on many fronts. (62,66) As one example, hepatic metabolism of fructose favors de novo lipogenesis. In turn, subsequent hepatic fat accumulation (steatosis) has been linked to insulin resistance and the metabolic syndrome. (51,67-70) On another front, the ability of fructose to elevate uric acid levels in addition to causing insulin resistance has been proposed to be a major mechanism behind cardiorenal diseases (71,72) and elevated BP. (71,73)
Studies Examining through the Early Decades the Role of Sugar Consumption in BP Regulation
In the 60's decade, table salt (sodium chloride), not table sugar (sucrose), was linked to BP elevations in light of the series of papers written by Hall and Hall. (74-77) The perception was that sucrose placed in the saline caused greater intake of sodium chloride resulting from a more favorable taste. The common belief at that time was that the increased sodium challenge, not the sucrose itself, was responsible for raised BP. Indeed, in follow up studies over immediately ensuing years, most investigators focused primarily on the role that rapidly absorbed carbohydrates might play in enhanced salt-promoted BP elevations.
By the end of the 70's decade, the results from a sparse number of studies were inconclusive in determining a direct role for sugar-induced BP elevations. (78-82) Emphasis was placed on salt and how sugar might influence its pressure effects rather than any direct modulation from the sugar itself. Nevertheless, the possibility that sugar-induced hypertension exists was still in play and clearer evidence was about to come forth at the beginning of the 80's.
In 1980, Srinivasan et al. fed 18 spider monkeys three diets: no added sodium chloride (NaCl), 3% NaCl, and 3% NaCl plus sucrose at 38% of calories. (83) An additional group assessing the effects of sucrose (38% of calories) alone with no supplementary NaCl was not included until a year later. (84) Unfortunately, BP was measured under sedation. After eight weeks of experimental feedings, the average BP of control monkeys were 142 mmHg + 2.4 (SEM); for NaCl 163 mmHg + 5.2 (SEM); for NaCl + sucrose 165.8 mmHg + 5.2 (SEM). The values for the last two groups were not significantly different from each other.
Also in 1980, Ahrens et al. examined the capability of sucrose substituted for starch to elevate BP . The basic diet consisted of fat (38%), protein (15%), lactose (7%) and the remaining 40% from different sucrose/starch ratios. Considering the sucrose/starch ratios, the five dietary groups set up were comprised of those receiving sucrose at 0,5,10,15, and 20% w/w balanced by added cornstarch. Five young male and five older female rats were selected for each group. Combining the different age and gender rats resulted in the following: 10 rats consuming the diet containing 20% sucrose showed mean systolic pressures changes after seven and 14 weeks --respectively 5.4 mmHg and 7.2 mmHg higher than the 10 rats receiving no additional sucrose.
In the same year, Preuss and Preuss reported the pressure effects of dietary sucrose and/or sodium on three sub strains of Wistar rats: spontaneously hypertensive (SHR), normotensive Wistar Kyoto (WKy), and normotensive American Wistar (WAm) rats. (24) Sucrose (10% w/v) and/or NaCl (1% w/v) were placed in the drinking water. The initial findings of the "salt effect" alone on systolic BP showed that the SHR and WKy were salt-sensitive and that the WAm were not. When sucrose was provided to the same SHR and WKy drinking saline, BPs rose noticeably in over one half the rats. 'Differently, WAm responded weakly to both sucrose and NaCl drinking solutions. The findings in the SHR and WKy could not be explained on more sodium ingestion or retention, and body weight remained similar among groups under the different conditions.
In another arm of the same report, sucrose alone in the drinking water brought on a significant increase in systolic BP of SHR--an average of 27 mmHg above the baseline (p<0.01); whereas, a group drinking saline alone showed a 10 mm Hg average increase above the baseline (p<0.05) . In the last group, sucrose plus saline resulted in the greatest elevation above baseline in SHR (45 mmHg, p<0.02) revealing a synergistic response. Clearer evidence that the presence of fiber can ameliorate the "sugar effect" became available later. (86, 88) This study set off a number of similar ones soon to follow that corroborated the existence of sugar-induced BP elevations. (89,90)
Following Three Decades (90s, 00s, 10s)
Over the following decades, numerous scientific papers appeared that strengthened the concept that dietary sugars and refined carbohydrates have a prominent role in everyday BP regulation. (5,7,91-101) Among the best examples are those concerned with the role of sugar containing beverages like soft drinks. As mentioned in our prior discussion, the tendency to consume sugar-containing soda free of any food effects, i.e., on an empty stomach, provides the most robust sugar challenge.
Correlation Between Insulin Resistance and Hyperinsulinemia and Elevated BP
Elevation of BP by sugars depends largely upon augmented insulin resistance stemming from excess intake. (1,2,42,51-55,102-104) Isocaloric exchanges of dietary sucrose for starch have long been known to bring on increases in fasting blood glucose and insulin levels in both humans (105,106) and rats. (107) This situation, i.e. elevated circulating glucose and insulin concentrations, soundly implies insulin resistance--a condition often linked to dietary imprudence. (42,51,52,108) Responding to insulin resistance from whatever cause, circulating levels of glucose rise and cause, at least initially, an eventual increase in insulin concentrations. (1,2) The usual result of this is that both glucose and insulin concentrations ascend concomitantly. Accordingly, insulin resistance, even in mild forms, can be approximated by utilizing circulating glucose and/or insulin levels. (52,109)
Therefore, we obtained data from relatively healthy volunteers, mostly females. These volunteers for clinical studies might receive in their baseline workup: BP measurements, body composition analyses, and assessment of blood chemistries such as circulating fasting levels of glucose. (55) Data on 151 subjects were obtained (Fig. 1). Significant positive correlations of systolic (p<0.001) and diastolic (p<0.001) BP were found when fasting glucose was used as the independent variable.
Interaction between Dietary Sugars and Table Salt
Rather than debating over the relative magnitude of the adverse effects that table salt and dietary sugars have on BP individually, a case could be made that both dietary factors should be considered together. (110) Solid evidence suggests that their interaction may result from an overlap between pathways through which table salt and sugars contribute to high BP. (24,111-114) Salt ingestion is associated with hypertension through volume expansion and insulin resistance. (115-117) Sugar intake, likewise, is linked to hypertension via augmented salt sensitivity, urinary sodium retention, and insulin resistance. (52,57,109,118,119) So, it is not surprising that circulating sodium concentrations correlate significantly positive with fasting glucose levels (n=298, p=0.034), (55,102) Fig. 2. Therefore it seems likely that salt and dietary sugars together can increase their respective individual BP measurements.
In conclusion, it is makes sense to consider that high sugar intake is associated with a greater risk of cardiovascular disease. (120) The interaction between common dietary sugars and table salt on BP control is a plausible postulate and should be prudently considered when planning the most advantageous prevention and treatment regimens to ameliorate the global crisis arising from damaging elevated BP levels. (110) Recent evidence concerning the range of normal BP suggests we need to keep our BP even lower than previously recommended to avoid a continuum of health risks. (55,121)
About the Author
Harry G. Preuss MD Department of Biochemistry, Georgetown University Medical Center, Washington, DC 20057
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by: Harry G. Preuss, MD
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|Author:||Preuss, Harry G.|
|Date:||Jun 1, 2018|
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