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As levels of diabetes, obesity, and other dietary issues increase (diabetes alone has increased 763% from 1935 to 1996 in the united states (Gross et al 2004)) studies have been conducted to investigate whether the 1,000% rise in the use of High Fructose Corn Syrup (HFCS) from 1967 to 2000 in the American food industry is a major contributor (Bray et al 2004).^{1  2} In this article, we will examine whether or not HFCS is truly a factor in this significant increase.

Early studies found that there were possible clinical explanations for metabolic differences derived from HFCS ingestion and other sweeteners; primarily that it did not trigger insulin creation and thereby was thought to not trigger satiety signals (Reiser et al 1989) (Elliott et al 2002) (Bray et al 2004) (Teff et al 2004) .^3 4 5 6  However, more recent studies have found no difference in resulting satiety in men or women resulting from HFCS, sucrose, or milk, (Soenen and Westerterp-Plantenga 2007) (Melanson et al 2008) (Akhavan and Anderson 2007),^7 8 9 and that HFCS yields similar metabolic responses to other caloric sweeteners. (Angelopoulos et al 2009),¹⁰ Stanhope et al 2008 and Melanson  et al 2007 determined that sucrose and HFCS do not have significantly different short-term metabolic effects,^11 12 and moderate levels (~1.5 grams of fructose per kilogram of body mass) of HFCS intake  does not cause ectopic lipid deposition or insulin resistance in healthy humans (Le et al 2006).¹³

Although HFCS is not itself responsible for the increase in dietary and metabolic disorders, other studies have demonstrated that increasing levels of excess energy consumption in general is a cause (Gross et al 2004).¹⁴  For thousands of years humans consumed fructose amounting to 16–20 grams per day, largely from fresh fruits (Gross et al 2004). ¹⁵ Westernization of diets has resulted in significant increases in food with added fructose, leading to typical daily consumptions amounting to 85–100 grams of fructose per day (Gross et al 2004). ¹⁶  For example, a 12 ounce Coke contains 39 grams of fructose and the USDA Recommended Daily Allowance allots for 32 grams of carbohydrates in a 2,000 calorie diet.¹⁷  A single 12 ounce Coke therefore contains significantly more than an individual’s entire excess dietary energy allowance for a day.  Raben et al 2002 found that people have a very difficult time compensating for increased levels of calories associated with increased sugar intake by lowering caloric intake elsewhere.¹⁸  While moderate ingestion of HFCS will not specifically cause harm to oneself, it is advisable to monitor and limit consumption as much as possible.

1. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity [↩]
2. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
3. Fructose, weight gain, and the insulin resistance syndrome [↩]
4. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity [↩]
5. Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women [↩]
6. Day-long glucose, insulin, and fructose responses of hyperinsulinemic and nonhyperinsulinemic men adapted to diets containing either fructose or high-amylose cornstarch [↩]
7. No differences in satiety or energy intake after high-fructose corn syrup, sucrose, or milk preloads [↩]
8. High-fructose corn syrup, energy intake, and appetite regulation [↩]
9. Effects of glucose-to-fructose ratios in solutions on subjective satiety, food intake, and satiety hormones in young men [↩]
10. The Effect of High-Fructose Corn Syrup Consumption on Triglycerides and Uric Acid [↩]
11. Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals [↩]
12. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women [↩]
13. A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans [↩]
14. Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment [↩]
15. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
16. Fructose, insulin resistance, and metabolic dyslipidemia [↩]
17. Carbohydrates [↩]
18. Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects [↩]

Kidney stones will effect around 5 percent of people in at some point in their life, and the rate is growing with time (Parmar 2004). ¹   Significant variation of occurrence exists between sexes; men develop stones twice as often as women at an average age of 30 while for women average age is bimodal with peaks at 35 and 55 (Parmar 2004).²   Once you have had one, you also have a very high chance of having another one as there is a re-occurrence rate of 50% over five years  (Borghi et al 1996).³  Although there is still somewhat of an evolving consensus around what the main cause is, literature points to treatment resistant micro-bacteria  (Çiftçioglu et al 1999) that combines with urine supersaturated with calcium compounds and uric acid (contributed by an individual’s diet), creating the kidney stone (Kajander et al 2003). ^4 5

An individual’s weight and family history have both been demonstrated to have a positive correlation with his or her risk of getting kidney stones (Taylor et al 2005) (Curhan et al 1997). ^6 7  However, lack of daily water intake has been demonstrated to be the greatest risk factor, and increasing one’s daily water intake is an easily preventative measure one can take to avoid getting stone’s in the first place (Borghi et al 1996). ⁸  Drinking at least 2.5 liters of water per day has been shown to change the consistency of urine, lowering it’s saturation level of calcium compounds, thereby preventing supersaturation and it’s associated buildups (Borghi et al 1996).⁹  This alone has been found to reduce reoccurred rates of kidney stones from 50% to 20% over a five year period (Borghi et al 1996). ¹⁰

Intake of other fluids have also been found to decrease instances of kidney stones in both sexes.  A study by Curhan et al (1998) found the following percentage of occurrence reductions in women for each 240-mL (8-oz) daily serving of the following fluids: caffeinated coffee – 10%, decaffeinated coffee – 9%, tea – 8%, and wine – 59%.¹¹  In contrast, a 44% increase in risk was seen for each 240-mL serving of grapefruit juice consumed daily (Curhan et al 1998).   In men the risk of stone formation decreased by the following percentages for each 240-ml (8-oz) daily serving of the following fluids:  caffeinated coffee 10%, decaffeinated coffee – 10%, tea – 14%,  beer – 21%, and wine – 39%. In contrast, a risk increased 35% for comparable servings of apple juice and 37% for grapefruit juice (Curhan et al 1996).¹²

Reducing one’s consumption of animal protein to less than 52g per day has also been shown to lower one’s risk of specific types of kidney stones (Breslau et al 1988).¹³  Increasing dietary calcium has been shown to lower risk for kidney stones in women (Borghi et al 2002) and men (Curhan et al 1993) and lowering your salt intake to less than 800 mg per day combined with lower intake of animal protein lowers men’s risk of re-occurrence by 18% (Borghi et al 2002).¹⁴  Also, vitamin B6 in doses of >40mg/day has been found to reduce incidences of kidney stones in women (Curhan et al 1999).¹⁵¹⁶  A recent study by Taylor et al (2004) determined that in men: sodium phosphorus, sucrose, phytate, vitamin B6, vitamin D, and supplemental calcium were not independently associated with risk for first time instances, while magnesium intake decreases and total vitamin C intake seems to increase the risk of kidney stones (Taylor et al 2004).¹⁷  While this research may appear to contradict the previous study by Borghi et al (2002), this study examined the combination of reduced salt and animal protein, which suggests that reducing animal protein consumption is a more important dietary change to aid in reduced kidney stone risk.¹⁸

1. Kidney stones [↩]
2. Kidney stones [↩]
3. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study [↩]
4. Nanobacteria: An infectious cause for kidney stone formation [↩]
5. Characteristics of nanobacteria and their possible role in stone formation [↩]
6. Obesity, Weight Gain, and the Risk of Kidney Stones [↩]
7. Family history and risk of kidney stones [↩]
8. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study [↩]
9. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study [↩]
10. Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study [↩]
11. Beverage Use and Risk for Kidney Stones in Women [↩]
12. Prospective Study of Beverage Use and the Risk of Kidney Stones [↩]
13. Relationship of Animal Protein-Rich Diet to Kidney Stone Formation and Calcium Metabolism [↩]
14. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria [↩]
15. Intake of Vitamins B6 and C and the Risk of Kidney Stones in Women [↩]
16. A Prospective Study of Dietary Calcium and Other Nutrients and the Risk of Symptomatic Kidney Stones [↩]
17. Dietary Factors and the Risk of Incident Kidney Stones in Men: New Insights after 14 Years of Follow-up [↩]
18. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria [↩]

Amalgam fillings, commonly used for the last century, are an alloy of approximately 50% mercury, 35% silver with other trace elements (Hahn et al 1989)¹.  Mercury is a versatile element, and is utilized in both organic and inorganic forms; both of which are toxic (Langford and Ferner 1999).² A study by Nylander et al (1987) demonstrated a statistical correlation between number of amalgam fillings  and amount of accumulated inorganic mercury in an individuals body. ³  Hahn et al (1989) found mercury vapor is released into the mouth by chewing action, and activities that increase this activity such as chewing gum and brushing teeth increase the level of mercury released.  Likely routes of uptakes of released vapors suggested in this study include inhalation, swallowing, and absorption through bone, tooth, and gum tissues in the mouth.  However, the actual amount of mercury absorbed into body tissue was undetermined, and the authors suggest more research is required to determine this.  ⁴  The results of this study suggest that there is an increase in mercury exposure in individuals with amalgam fillings, however,  it is necessary to ascertain both how much mercury is actually absorbed, as well as the effect this mercury has on an individual.

Myriad results have been found in regards to determining the effects of absorbed mercury from amalgam fillings.  Sandborgh-Englund et al (1996)  and Bates (2006) found no evidence of renal toxicity, chronic fatigue syndrome, reproductive, or other chronic diseases  from mercury absorbed from amalgams, but a evidence of susceptibility to Alzheimer’s, Multiple Sclerosis, and Parkinson’s from mercury absorbed from amalgams. ^5 6  In addition, Grandjean et al (1997) found that individuals treated for self reported amalgam related psychotic disorders responded equally to a mercury purging drug in both treatment and placebo groups, while those in the treatment group actually expelled much higher levels of mercury in their urine.⁷  Further study is required for a more definitive answer to whether or not amalgam fillings should be considered a health threat, however, the aforementioned studies have demonstrated that chronic physiological disorders are not associated with amalgams while neurological disorders can be.

1. Dental “silver” tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis [↩]
2. Toxicity of mercury [↩]
3. Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings [↩]
4. Dental “silver” tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis [↩]
5. No evidence of renal toxicity from amalgam fillings [↩]
6. Mercury amalgam dental fillings: an epidemiologic assessment [↩]
7. Placebo Response in Environmental Disease: Chelation Therapy of Patients With Symptoms Attributed to Amalgam Fillings [↩]