Soda and Obesity

type 2 diabetes, obesityWhile a major study relating soda and obesity was done in California, the hypothesis, observations and outcomes are applicable to all the states of the Union.  More than half the adolescents in that state and almost a fourth of the adults treat themselves to at least one sweetened beverage every day.  One of the concerns expressed by UCLA researchers is that the serving size has grown from an average of 6.5 ounces and eighty-eight calories in the 1950’s to 20 ounces and two hundred sixty-six calories by the 2000’s.  In fast food restaurants in 2003, the average serving was 23 ounces (almost 300 calories).  These added caloric sweeteners, including high fructose corn syrup, are not only markers of a poor diet, but also are associated with overweight and obesity in all age groups.

The UCLA Health Policy Research Brief from September, 2009, reports from its data that, “Adults who drink soda occasionally (not every day) are 15% more likely to be overweight or obese, and adults who drink one or more sodas per day are 27% more likely to be overweight or obese than adults who do not drink soda, even when adjusting for poverty status and race/ethnicity.”  Even though the prevalence of overweight in children is lower than in adults, the rates among children have increased more.  In fact, overweight has tripled in teenagers and quadrupled in those from six to eleven years old in the last three decades.  In California the cost of obesity approaches twenty-one billion dollars a year, burdening families, employers and the health care industry.  The study comments that, “California spends more public and private money on the health consequences of obesity than any other state.”  To compound the matter, the article admits that “…drinking soda is also associated with increased risk for type 2 diabetes.”

One third of American adults are obese. Their health care costs $1500 more a year than it does for an average-weight person.  The Center for Disease Control announced in July, 2011, that obesity in the entire United States costs $147 billion a year in direct medical costs.  Dr. Thomas R. Frieden, director of the CDC, said the problem is “getting worse rapidly.  The average American is now 23 pounds overweight.”  For Medicare, the cost of obesity is 72% greater just for prescription drugs.  The CDC says that one in three children born in 2000 will develop diabetes.  How did we get there?  Diet.  Does the rest of the world share the problem?  Yes.  Where does the blame go?  White flour, white sugar, high fructose corn syrup, soft drinks and fast food.

Whether it gets marketed as corn sugar or as high fructose corn syrup, which is what it is, this commodity is not equal to other sweeteners when it comes to weight gain.  HFCS costs less than table sugar because, being liquid, it’s easier to transport and blend.  It’s sweeter than sucrose (table sugar), so less is needed, and it’s cheaper because of a combination of corn subsidies and sugar tariffs and quotas.  Cheap corn, in fact, is the building block of the fast-food nation.  Cheap corn created the chubby 20-ounce bottle of soda we have today.

High fructose corn syrup commonly is 55% fructose and 45% glucose, somewhat different from the 50-50 mix in table sugar, where one fructose molecule is attached to one glucose molecule.  Some HFCS may be as high as 80% fructose.  Since all sugars contain four calories per gram, there must be something else about fructose that matters.  Fructose is metabolized more rapidly that glucose, flooding metabolic pathways and increasing triglyceride storage.   It doesn’t spur the production of insulin or leptin, the hormone that sequesters appetite.  The body then lacks satiety.  This elevates serum triglycerides and increases fat storage.  Since it may have less impact on appetite than glucose, fructose contributes to weight gain.  Ingesting lots of fructose may also reduce insulin sensitivity.  (Beck-Nielsen, 1980)

Soft drink consumption has more than doubled in the twenty years from 1977 to 1997.  Not surprisingly, obesity followed the same trend. Cause and effect? It’s been estimated that for each additional sweet drink consumed per day, the odds of obesity increase by sixty percent.  A study of more than fifty thousand nurses by Harvard compared time periods from 1991-1995 and 1995-1999, and found that women whose soda consumption increased had bigger rises in body-mass index than those who drank less or the same amounts of soda. Fast food seems to go well with it.  Unhealthy foods get along nicely with each other.

The debate between the soft drink industry and the health nuts is ongoing.  People who consume lots of fresh-squeezed juices, vegetables and fruits are not the same group that consumes soda and cold cut sandwiches.  The daily calories from soft drinks account for almost a fourth of the recommended daily intake for many Americans, who drink almost fifty-six gallons of soda a year.

In case you’re interested, more than 30% of Americans are obese. More than 24% of Mexicans, 23% of British, 22% of Slovakians, 22% of Greeks and Australians, 21% of New Zealanders, and 15% of Czechs, but only 3% of Japanese and Koreans. Go figure. Obesity, by the way, means being more than 20% above ideal weight for height.


UCLA Health Policy Research Brief
September 2009
Bubbling Over: Soda Consumption and Its Link to Obesity in California
Susan H. Babey, Malia Jones, Hongjian Yu and Harold Goldstein

In California, 62% of adolescents ages 12-17 and 41% of children ages 2-11 drink at least
one soda or other sweetened beverage every day. In addition, 24% of adults drink at least
one soda or other sweetened beverage on an average day. Adults who drink soda occasionally
(not every day) are 15% more likely to be overweight or obese, and adults who drink one or
more sodas per day are 27% more likely to be overweight or obese than adults who do not
drink soda, even when adjusting for poverty status and race/ethnicity.

The prevalence of overweight and obesity has increased dramatically in both adults
and children in the last three decades in the United States. In the 1970s, about 15% of
adults were obese and by 2004 the rate had climbed to 32%.1 Although the prevalence of
overweight among children is lower than among adults, the rates among children and
adolescents have increased considerably more. The prevalence of overweight and obesity
nearly tripled among 12-19 year olds and more than quadrupled among 6-11 year olds
in the last three decades.

In California, 21% of adults are currently obese and an additional 35% are overweight. Among adolescents, 14% are obese and another 16% are overweight.2 Similar to national trends, the trend in California is toward increasing weight in both adults and adolescents.3 Each year in California, overweight and obesity cost families, employers, the health care industry and the government $21 billion.4 California spends more public and private money on the health consequences of obesity than any other state.5

Overweight and obesity are associated with serious health risks. In children and adolescents, overweight and obesity are associated with increased risk for cardiovascular disease indicators including high total cholesterol, high blood pressure, and high fasting insulin, an early indicator of diabetes risk.6 In addition, overweight children and adolescents are more likely to be overweight or obese as adults.7 In adults, overweight and obesity are associated with increased risk for diabetes, heart disease, stroke, some types of cancer and premature death.1, 8, 9

Drinking sweetened beverages such as soda and fruit drinks that have added caloric sweeteners (e.g., sucrose, high fructose corn syrup) is one marker of a poor diet, and is
associated with overweight and obesity in people of all ages.10-13 A number of studies have found that greater consumption of sweetened beverages is associated with overweight and obesity among both adults and children.12-19 In addition, randomized controlled trials that examine the impact of reducing intake of sweetened beverages on weight indicate
that reducing consumption of soda and other sweetened drinks leads to reductions in
overweight and obesity.20, 21 Among adults, drinking soda is also associated with increased risk for type 2 diabetes.13 Moreover, drinking sweetened beverages has
increased, and it is now more common than ever, particularly among adolescents.22
Between 1977 and 2002 Americans increased their calorie intake from soft drinks by
228%.23 Portion sizes have also increased from an average serving size of 6.5 fl oz (88 calories) in the 1950s, to 12 fl oz (150 calories), 20 fl oz (266 calories), and even larger portion sizes common today.24-26 The average serving size of soft drinks in fast food restaurants in 2002 was 23 fl oz (299 calories), with some chains now commonly selling soft drinks in 32 to 64 fl oz portions (416 to 832 calories, respectively).27 Sweetened beverages are a significant contributor to total caloric intake, especially for children and adolescents, and they lack the nutrients our bodies need.24, 26, 28

Additionally, eating habits established in childhood are important determinants of
eating habits as adults.29, 30

Am J Clin Nutr February 1980 vol. 33 no. 2 273-278
Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects
H Beck-Nielsen, O Pedersen and HO Lindskov

We have studied whether the sucrose-induced reduction of insulin sensitivity and cellular insulin binding in normal man is related to the fructose or the glucose moiety. Seven young healthy subjects were fed their usual diets plus 1000 kcal extra glucose per day and eight young healthy subjects were fed their usual diets with addition of 1000 kcal extra fructose per day. The dietary regimens continued for 1 week. Before change of diet there were no statistically significant differences between body weight and fasting plasma concentrations of glucose, insulin, and ketone bodies in the two groups studied. High- glucose feeding caused no significant changes in insulin binding or insulin sensitivity whereas high-fructose feeding was accompanied by a significant reduction both of insulin binding (P less than 0.05) and insulin sensitivity (P less than 0.05). The changes in insulin binding and insulin sensitivity correlated linearly (r = 0.52, P less than 0.01). We conclude that fructose seems to be responsible for the impaired insulin binding and insulin sensitivity induced by sucrose.

Medscape J Med. 2008;10(8):189. Epub 2008 Aug 12.
Soft drinks and weight gain: how strong is the link?
Wolff E, Dansinger ML.
Boston University School of Medicine, Boston, Massachusetts, USA. [email protected]

Soft drink consumption in the United States has tripled in recent decades, paralleling the dramatic increases in obesity prevalence. The purpose of this clinical review is to evaluate the extent to which current scientific evidence supports a causal link between sugar-sweetened soft drink consumption and weight gain.

MEDLINE search of articles published in all languages between 1966 and December 2006 containing key words or medical subheadings, such as “soft drinks” and “weight.” Additional articles were obtained by reviewing references of retrieved articles, including a recent systematic review. All reports with cross-sectional, prospective cohort, or clinical trial data in humans were considered.

Six of 15 cross-sectional and 6 of 10 prospective cohort studies identified statistically significant associations between soft drink consumption and increased body weight. There were 5 clinical trials; the two that involved adolescents indicated that efforts to reduce sugar-sweetened soft drinks slowed weight gain. In adults, 3 small experimental studies suggested that consumption of sugar-sweetened soft drinks caused weight gain; however, no trial in adults was longer than 10 weeks or included more than 41 participants. No trial reported the effects on lipids.

Although observational studies support the hypothesis that sugar-sweetened soft drinks cause weight gain, a paucity of hypothesis-confirming clinical trial data has left the issue open to debate. Given the magnitude of the public health concern, larger and longer intervention trials should be considered to clarify the specific effects of sugar-sweetened soft drinks on body weight and other cardiovascular risk factors.  PMID: 18924641

Diabetes Care. 2010 Nov;33(11):2477-83. Epub 2010 Aug 6.
Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis.
Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB.

Department of Nutrition, Harvard School of Public Health, and Department of Medicine, Brigham and Women’s Hospital, Boston, MA, USA.

Consumption of sugar-sweetened beverages (SSBs), which include soft drinks, fruit drinks, iced tea, and energy and vitamin water drinks has risen across the globe. Regular consumption of SSBs has been associated with weight gain and risk of overweight and obesity, but the role of SSBs in the development of related chronic metabolic diseases, such as metabolic syndrome and type 2 diabetes, has not been quantitatively reviewed.

We searched the MEDLINE database up to May 2010 for prospective cohort studies of SSB intake and risk of metabolic syndrome and type 2 diabetes. We identified 11 studies (three for metabolic syndrome and eight for type 2 diabetes) for inclusion in a random-effects meta-analysis comparing SSB intake in the highest to lowest quantiles in relation to risk of metabolic syndrome and type 2 diabetes.

Based on data from these studies, including 310,819 participants and 15,043 cases of type 2 diabetes, individuals in the highest quantile of SSB intake (most often 1-2 servings/day) had a 26% greater risk of developing type 2 diabetes than those in the lowest quantile (none or <1 serving/month) (relative risk [RR] 1.26 [95% CI 1.12-1.41]). Among studies evaluating metabolic syndrome, including 19,431 participants and 5,803 cases, the pooled RR was 1.20 [1.02-1.42].

In addition to weight gain, higher consumption of SSBs is associated with development of metabolic syndrome and type 2 diabetes. These data provide empirical evidence that intake of SSBs should be limited to reduce obesity-related risk of chronic metabolic diseases.

J Public Health Policy. 2004;25(3-4):353-66.
The obesity epidemic in the United States.
Morrill AC, Chinn CD.
Capacities Inc., Watertown, Massachusetts 02471, USA. [email protected]

We describe the epidemic of obesity in the United States: escalating rates of obesity in both adults and children, and why these qualify as an epidemic; disparities in overweight and obesity by race/ethnicity and sex, and the staggering health and economic consequences of obesity. Physical activity contributes to the epidemic as explained by new patterns of physical activity in adults and children. Changing patterns of food consumption, such as rising carbohydrate intake–particularly in the form of soda and other foods containing high fructose corn syrup–also contribute to obesity. We present as a central concept, the food environment–the contexts within which food choices are made–and its contribution to food consumption: the abundance and ubiquity of certain types of foods over others; limited food choices available in certain settings, such as schools; the market economy of the United States that exposes individuals to many marketing/advertising strategies. Advertising tailored to children plays an important role.  PMID: 15683071

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Salt May Not Be As Bad As They Say…Or Is It?

regulate salt intakeUsing a sufficiently large set of data, the Cochrane Library, a highly respected international collaboration of evidence-based medicine reviews, was able to draw startling conclusions about the association of salt intake with high blood pressure and cardiovascular risks. After looking at almost 6,500 people, comprising several well-conducted studies, Cochrane found that, for CVD mortality and all-cause mortality in persons with normal or elevated blood pressure, there is no strong evidence for restricting salt intake.

The American Journal of Hypertension reported Cochrane’s findings in July of 2011, stating that, “Although meta-analyses of randomized controlled trials of salt reduction report a reduction in the level of blood pressure, the effect of reduced dietary salt on cardiovascular disease events remains unclear.”  However, it was also found that salt reduction “was associated with reductions in urinary salt excretion…and reductions in systolic blood pressure between 1 and 4 mm Hg.”  Additionally, relative risk did not show evidence of any effect of salt reduction on cardiovascular episodes in people with normal BP, but noted that, “salt restriction increased the risk of all-cause mortality in those with heart failure.”

The Cochrane reviewers admitted that, despite collecting more data than ever before, there is still no definitive proof that salt reduction will have beneficial effects on all-cause mortality or on the risk of cardiovascular disease.  At the same time, Katherine Jenner, campaign director of the Consensus Action on Salt and Health (CASH), disputes these findings, adding that there are no trials to account for other chronic exposures, such as smoking and being overweight, and eating too few fruits and vegetables.  She stated strongly that it would be unethical to expose humans to a long period of high salt intake merely to satisfy the curiosity of researchers.  To add to this confusion, the Cochrane leader, Rod Taylor, said that large benefits were not seen because salt reduction was sufficiently minimal as to cloud significant effects on BP and heart disease.  Huh?

Prior to the development of refrigeration, salt was necessary for the preservation of food.  Milk was made into cheese using salt, and fish was salted to keep it for long periods.  Eating as we do, many of us accumulate more salt and water than the kidneys can handle.  Some folks have genes that control cellular channels, enzymes and hormones at various places in the kidneys, conserving salt to enable adaptation to hot and dry climates.  If water and salt were scarce, as would often be the case in mankind’s early days, the kidney would conserve salt to hold the water that would become sweat, which would evaporate from the skin and cool the body enough to keep temperature stable.  Without sweat the body would overheat.  These genes that were important to early mankind never stopped doing their job, regardless of climate.  About 20% of us will continue to reabsorb salt as long as excessive amounts are ingested.  Salt retains water through osmosis.  It also promotes thirst.  Why else would there be a bowl of salty pretzels or nuts on the bar?

Excess salt keeps circulatory volume higher than it needs to be, putting extra fluid pressure on blood vessel walls.  The walls react to this stress by getting thicker and narrower, leaving less space for the fluid already cramped inside, thereby raising resistance to flow and increasing the pressure needed to get it moving.  Because the heart has to pump against greater pressure, it can grow larger, just like the skeletal muscles subjected to heavy pressure from lifting weights.  Whatever excess pressure is exerted on the kidneys causes those organs to compromise their delicate filtration system, leading to disease.

Beyond reducing blood pressure, a low sodium intake improves the dilation of the blood vessels and consequently improves heart function.  Dilation of blood vessels is considerably greater in a low-sodium environment. (Dickinson. 2009)  Systolic pressure will drop, as well.

At a time when the U.S. advocates lowering salt intake from 2,300 mg a day to 1,500 mg a day, the Europeans are happy to see their intake lowered to 5,000 mg a day.  Considering that the typical European intake seems to be around 9,000 to 12,000 mg a day, that is quite a change.  Naturally, they would see a drop in blood pressure.  (He and Burnier. 2011)  Salt sensitivity is subjective, though, and not everyone would have a BP spike because of intake.

But now there might just be way to help control salt-induced blood pressure elevation. Researchers at Loyola University, under the direction of Dr. Paul Whelton, learned that the ratio of sodium to potassium is a more important indicator of cardiovascular problems than either salt or potassium alone.  (Whelton and Cook. 2009)  Little studied, potassium is the element on the other side of the cell membrane from sodium. Most of us are potassium deficient, consuming far less than the 4,700 mg a day that is suggested. The recommended 9 to 13 servings of fruits and vegetables a day, the most reliable sources of this mineral, is uncommon in the contemporary diet.  A high sodium to potassium ratio can be predictive of future coronary episodes; a low one, the opposite.  In his study, Dr. Whelton says that 2,300 milligrams should be the maximum sodium intake a day for those less than 30 years old, half that for those who are older.

Sodium is not salt, and salt is not sodium. About 40% of salt is sodium, the remainder being chloride, the chemical of which stomach acid is made.

For some of us, salt might be off the hook. For others of us, it might be a gremlin. It can be hidden in frozen dinners, some cereals, vegetable juice, canned vegetables and soups, sauces and marinades, snacks, and condiments. Potassium, on the other hand, is friendly to all. Jing Chen and his colleagues agree. (Chen. 2008)


Am J Hypertens. 2011 Jul 6. doi: 10.1038/ajh.2011.115. [Epub ahead of print]
Reduced Dietary Salt for the Prevention of Cardiovascular Disease: A Meta-Analysis of Randomized Controlled Trials (Cochrane Review). Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S.

Cochrane Database of Systematic Reviews 2011, Issue 7.
Reduced dietary salt for the prevention of cardiovascular disease.
Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S.

Am J Clin Nutr February 2009 vol. 89 no. 2 485-490
Effects of a low-salt diet on flow-mediated dilatation in humans
Kacie M Dickinson, Jennifer B Keogh, Peter M Clifton

Arch Intern Med. 2008;168(16):1740-1746.
Association Between Blood Pressure Responses to the Cold Pressor Test and Dietary Sodium Intervention in a Chinese Population
Jing Chen, MD, MSc; Dongfeng Gu, MD, MSc; Cashell E. Jaquish, PhD; et al

Arch Intern Med. 2009;169(1):32-40.
Joint Effects of Sodium and Potassium Intake on Subsequent Cardiovascular Disease
The Trials of Hypertension Prevention Follow-up Study
Nancy R. Cook, ScD; Eva Obarzanek, PhD; Jeffrey A. Cutler, MD; Julie E. Buring, ScD; Kathryn M. Rexrode, MD; Shiriki K. Kumanyika, PhD; Lawrence J. Appel, MD; Paul K. Whelton, MD

Eur Heart J. 2011 Jun 23. [Epub ahead of print]
Nutrition in cardiovascular disease: salt in hypertension and heart failure.
He FJ, Burnier M, Macgregor GA.

Wolfson Institute of Preventive Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Calorie Restriction Extends Lifespan

calorie restrictionCalorie restriction (CR) in animals extends longevity by a considerable margin. Both primary and secondary aging processes are decelerated by limiting foods to those that are high in nutrients and relatively low in calories. Studies on humans are only now in progress, while those in animals have been unfolding for a few years. One of the boons of CR is a lowered core body temperature, which is that at which all physiological activity is most efficient. Not only this, but also fat reduction and consequent cardiac health can defer the foibles and imperfections of old age.

Studies at Washington University (St. Louis, MO) and the U. of California at San Francisco, sponsored in part by the Calorie Restriction Society, have found that” (calorie) restriction in animals seems to be the fountain of youth…” Studies on people may or may not yield the same results, primarily because free-living humans are not accepting of the same externally imposed restrictions as are endured by the animals. Human variables that need to be addressed include alterations in cognitions, behaviors, responses to stressors, and effects on other markers of health. However, humans have shown some of the same “…adaptations that are…involved in slowing primary aging in rats and mice.” Most notable here is a reduction in the inflammatory markers known as C-reactive protein and Tumor Necrosis Factor-alpha.

Primary aging is the gradual and inevitable process of physical deterioration that occurs throughout life.  You know, the aches and pains, the slowed movements, the loss of 20-20 vision, decreased resistance to infections, impaired hearing, and the rest of the baggage.  Secondary aging results from diseases and poor health practices (read lifestyle) that include smoking, torpor, booze and obesity, all of which can contribute to diseases in the first place.

Does CR work in people?  Yes, as long as it is reasonable…and that varies from person to person.  Decreasing calorie intake by only a few hundred can make a significant difference in health and longevity by reducing body fat, lowering blood pressure and cholesterol, and avoiding degenerative diseases, such as diabetes and heart disease.  Don’t forget about lowered body temperature, where the Washington University researchers learned that life expectancy was increased in animals. (Soare, 2011)  Of course, we can’t definitely tell how this affects people because we don’t know when each is programmed to die.  It is such, however, that family history of salubrious long life can be predictive of an individual’s longevity.

You might be interested to know that a nutritional supplement demonstrates an effect that mirrors calorie restriction.  We advise that you not yet jump for joy without the realization that this needs to be approached sensibly, which means being attentive to calorie intake. You can’t go wild on doughnuts, white flour bagels, ice cream and other culinary nonsense. You see, the mechanism behind calorie restriction’s success is not completely understood, but it is presumed that a protein called sirtuin is responsible for control of the aging process, and that CR directs the activity of sirtuin. Part of the aging procedure involves cellular stress, particularly in the mitochondria, the power plants of the cell that make energy. If we can slow down oxidation by ramping up the mitochondria’s defense mechanisms and simultaneously inhibiting the attack of reactive oxygen species, then we might be able to stave off the pangs of aging.  How do we do that without restriction of calories?  What supplement is held in such high regard? Resveratrol, the red wine polyphenol!

Independent of each other, Zoltan Ungvari (2009) and Thimmappa Anekonda (2006) discovered that resveratrol may have therapeutic value in the treatment of metabolic and neuronal diseases, based at least partially on the activity of sirtuin.  What is known about resveratrol’s mechanism of action is that it encourages the sirtuin homologue SIRT1 to ply its trade as a cellular regulator, where it slows down metabolism and any stimulatory reactions to environmental toxins, thus placing an organism into a defensive state so it can survive adverse circumstances.  Tobacco smoke-induced oxidative stress even becomes minimized.

We are individuals with different needs and responses to interventions, whether dietary or medical.  You will differ in your response to calorie restriction from your twin. You will differ in your response to resveratrol, if that is the route you choose.  But it seems more than likely you will experience a strengthened immune system, heightened energy, a healthier reproductive system, increased stamina…and looser trousers.


Exp Gerontol. 2007 Aug;42(8):709-12. Epub 2007 Mar 31.
Caloric restriction in humans.
Holloszy JO, Fontana L.

Toxicol Pathol. 2009;37(1):47-51. Epub 2008 Dec 15.
Caloric restriction and aging: studies in mice and monkeys.
Anderson RM, Shanmuganayagam D, Weindruch R.

Aging (Albany NY). 2011 Apr;3(4):374-9.
Long-term calorie restriction, but not endurance exercise, lowers core body temperature in humans.
Soare A, Cangemi R, Omodei D, Holloszy JO, Fontana L.

Free Radic Biol Med. 2011 Apr 22. [Epub ahead of print]
The controversial links among calorie restriction, SIRT1, and resveratrol.
Hu Y, Liu J, Wang J, Liu Q.

Am J Physiol Heart Circ Physiol. 2008 Jun;294(6):H2721-35. Epub 2008 Apr 18.
Vasoprotective effects of resveratrol and SIRT1: attenuation of cigarette smoke-induced oxidative stress and proinflammatory phenotypic alterations.
Csiszar A, Labinskyy N, Podlutsky A, Kaminski PM, Wolin MS, Zhang C, Mukhopadhyay P, Pacher P, Hu F, de Cabo R, Ballabh P, Ungvari Z.

Am J Physiol Heart Circ Physiol. 2009 Nov;297(5):H1876-81. Epub 2009 Sep 11.
Resveratrol attenuates mitochondrial oxidative stress in coronary arterial endothelial cells.
Ungvari Z, Labinskyy N, Mukhopadhyay P, Pinto JT, Bagi Z, Ballabh P, Zhang C, Pacher P, Csiszar A.

Brain Res Rev. 2006 Sep;52(2):316-26.
Resveratrol–a boon for treating Alzheimer’s disease?
Anekonda TS.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Blood Pressure And Body Fat

sphygmomanometerIf you’re in the upper part of your normal weight range or are outright overweight, you might want to do something about it, especially if you’re getting up there in age.  The relationship between being overweight and having high blood pressure is well-established.

The upper part of the normal blood pressure range can be a danger zone for heart attack and stroke.  Investigators at Kaiser Permanente, in Portland, Oregon, looked at almost 600 men and women who were ten to sixty-five percent above their ideal weight, and who had slightly elevated blood pressure.  All were given weight reduction counseling, and later were compared to a like-sized group who received no such guidance.  It was found that a ten-pound weight loss effected a drop in diastolic (bottom number) blood pressure by 2.7 mm of mercury, which doesn’t sound like a lot, but which is significant.  For those who dropped twenty pounds, diastolic pressure dropped by 7 mm of Hg.  During this 3-year study, those who managed to keep the weight off also managed to keep their blood pressure under control, as opposed to the control group.  “Clinically significant long-term reductions in blood pressure and reduced risk for hypertension can be achieved with even modest weight loss” is the conclusion.  (Stevens. 2001)

Though a decade old, the cited study is pertinent.  The dietary habits of Americans are paving a road to dereliction by creating serious health concerns that include obesity, diabetes, CVD, and hypertension.  For every pound of fat above your ideal weight, you might be adding miles of blood vessels.  Although fat doesn’t need the vasculature that muscle does, it needs to be fed nonetheless.  If you were to add another hundred feet to your garden hose, you’d notice the water dripping out the end instead of flowing with purpose.  Unless you have a pump, you’ll not likely increase water pressure.  Your heart, on the other hand, will notice a need for increased pressure to get blood to the other end of the line and will do just that—increase the pressure.  If this goes on for too long, it just might start giving you trouble.

The Dietary Approach to Stop Hypertension (DASH) has been deemed an effective management tool.  Lifestyle modifications and salt reduction, along with a diet filled with fruits and vegetables, nuts and seeds, eliminating / limiting saturated and trans-fats and empty calories, was found to be effective in reducing blood pressure by considerable margins.  Those with the highest blood pressure realized the greatest benefits.  (Kolaska.  1999)  Exercise alone can lower blood pressure, but it’s not going to happen until you do it.  Combined with a behavioral weight loss program, even a modicum of exercise will show an enhanced effect.  (Blumenthal.  2000)  Health of the entire cardiovascular system is at stake, and the rewarded decrease in ventricular mass and wall thickness should be motivation enough to get an overweight hypertensive guy movin’ and shakin’.  The improvements in peripheral vascular health are also measurable, and conditions such as peripheral arterial disease may be forestalled.  (Bacon.  2004)

The development of obesity causes significant changes inside the body, things you can’t see.  Extra blood vessel formation is one such change.  And the accumulation of fat around the middle and the accompanying elevation in blood pressure may change lifestyle in an unwanted direction.


Stevens VJ, Obarzanek E, Cook NR, Lee IM, Appel LJ, Smith West D, Milas NC, Mattfeldt-Beman M, Belden L, Bragg C, Millstone M, Raczynski J, Brewer A, Singh B, Cohen J;
Trials for the Hypertension Prevention Research Group.
Long-term weight loss and changes in blood pressure: results of the Trials of Hypertension Prevention, phase II.
Ann Intern Med. 2001 Jan 2;134(1):1-11.

Kolasa KM.
Dietary Approaches to Stop Hypertension (DASH) in clinical practice: a primary care experience.
Clin Cardiol. 1999 Jul;22(7 Suppl):III16-22.

Blumenthal JA, Sherwood A, Gullette EC, Babyak M, Waugh R, Georgiades A, et al
Exercise and weight loss reduce blood pressure in men and women with mild hypertension: effects on cardiovascular, metabolic, and hemodynamic functioning.
Arch Intern Med. 2000 Jul 10;160(13):1947-58.

Bacon SL, Sherwood A, Hinderliter A, Blumenthal JA
Effects of exercise, diet and weight loss on high blood pressure.
Sports Med. 2004;34(5):307-16.

Lijnen HR.
Angiogenesis and obesity
Cardiovasc Res (2008 May 1); 78 (2): 286-293.

Blumenthal JA, Babyak MA, Hinderliter A, Watkins LL, Craighead L, et al
Effects of the DASH diet alone and in combination with exercise and weight loss on blood pressure and cardiovascular biomarkers in men and women with high blood pressure: the ENCORE study
Arch Intern Med. 2010 Jan 25;170(2):126-35.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Cold Weather Coronary Episodes

snowblowerThe way the body responds to low temperatures involves more than comfort. Cold temperatures cause arteries to tighten, restricting blood flow and reducing the oxygen supply to the heart, all of which can set the stage for a cardiac event. The heart has to work harder in the cold weather to keep the body warm, especially in the morning when blood pressure is on the upswing. The “blood pressure surge” just before waking is higher in the winter than at other times of the year. The tight management of blood pressure and cardiovascular health requires careful attention, but more so when the thermometer drops.

Since global climate change has been realized, more because of Earth’s orbital fluctuations than man’s dominion over its resources, interest has grown in the relationship between weather and health.  Measures of mortality have seen a decline when temperatures increase from the coldest days up to a certain point, above which mortality increases with temperature.  Detrimental effects of both hot and cold days also have been associated with cardiovascular mortality.  But it appears that winter has the most impact on circadian rhythm and disturbances in homeostasis that may lead to coronary episodes.

At London’s School of Hygiene and Tropical Medicine, researcher Krishnan Bhaskaran and his team found, “…a broadly linear relation between temperature and myocardial infarction…” whereby “…each 1° C reduction in daily mean temperature was associated with a 2.0% cumulative increase in risk of myocardial infarction over the current and following 28 days, the strongest effects being estimated at intermediate lags of 2-7 and 8-14 days..” (Bhaskaran.  2010)

Do bad things happen only to other people?  Most of us are guilty of the “it-can’t-happen-to-me” syndrome.  But could we be right?  This study mentions that, “the risk of infarction in vulnerable people might be reduced by the provision of targeted advice and other interventions, triggered by forecasts of lower temperatures.”  (Ibid.) The operative term here is vulnerable people.”  That deserves a sigh of relief, but not until you determine if you are in or out of that group.  However, the study points out that the adverse effect of the cold temperatures may linger for as long as two weeks.  Keep that in mind.  If you smoke, you’re vulnerable.  Got high blood pressure?  You’re vulnerable.  Lousy diet and nix on the exercise bit?  Yep, vulnerable.  How about being a type A personality with a high-stress lifestyle, or skipping a few visits with the dentist, or being large enough to have your own zip code?  Yup.  You’re in.  Now that you know, what’re you gonna do about it?

Mastering your Self can change the odds much in your favor.  It’s true that additional studies need to be conducted to ascertain the measures that could be taken to reduce risk for cold-weather coronary episodes, but there’s no reason not to start making changes right away.

Meteorological factors that include heavy snowfalls were examined in Scandinavia to look for any implications in cardiac events.  It was found that myocardial infarction (MI) increased especially in people older than 65, but not necessarily in younger groups, when the temperature dropped and the snowfall was heavy.  However, prudent behaviors, such as dressing for the conditions and delaying snow removal until the afternoon, could excuse a considerable number of people from cardiac episodes.  (Hopstock.  2011).  Similar work done by the Mayo Clinic has documented low-temperature peaks in coronary heart disease, suggesting that temperatures below 0° C are associated with sudden cardiac deaths. (Gerber. 2006).

Hypertension prevalence increases in the cold weather and in cold regions of the world, and that can trigger an event.  Animals exposed to these conditions exhibit cardiac hypertrophy (enlargement of the heart) and overactivity of the sympathetic nervous system, which is activated in stressful states and elevates heart rate and narrows blood vessels, thereby spiking blood pressure and setting the stage for an unwelcome happening.  (Sun. 2010).  The proteins designed to constrict blood vessels are especially sensitive to frigid temperatures.  (Chen. 2006).  Strangely, winter temperatures in Sicily hover near 60° F, yet researchers there have found seasonal peaks in infarction-related hospital admissions.  (Sicily’s latitude is very close to that of Washington, DC.) Humidity was included there as a partner in crime.  (Abrignani. 2009)  You’d expect cold weather to be a causative factor in Switzerland, and you won’t be surprised to learn that heavy winds are also implicated, while snowfall and rainfall have shown inconsistent effects.  (Goerre. 2007).

Morning blood pressure is typically higher than later in the day, so taking your medication in the evening may be suggested.  Dressing for the weather is just as important, and warming the air you breathe through a scarf might be a good idea.  Eliminating tobacco and being careful about alcohol intake can keep blood pressure lower.  Waiting for the sun to get higher in the sky, and for the temperature to rise above early-morning freeze, may alleviate cardiovascular stress.

If latitude is considered, it seems that any place outside the tropics is fingered as a winter time hazard for cardiac health.  The body’s ability to manufacture vitamin D from exposure to the sun is compromised at that time of year.  Since certain conditions are prevalent in the winter, when the angle of the sun is low, maybe vitamin D has something to do with it.  Hmm.


Krishnan Bhaskaran, Shakoor Hajat, Andy Haines, Emily Herrett, Paul Wilkinson, Liam Smeeth
Short term effects of temperature on risk of myocardial infarction in England and Wales: time series regression analysis of the Myocardial Ischaemia National Audit Project (MINAP) registry
BMJ 2010; 341:c3823

Hopstock LA, Fors AS, Bønaa KH, Mannsverk J, Njølstad I, Wilsgaard T.
The effect of daily weather conditions on myocardial infarction incidence in a subarctic population: the Tromso Study 1974-2004.
J Epidemiol Community Health. 2011 Jun 6.

Gerber Y, Jacobsen SJ, Killian JM, Weston SA, Roger VL.
Seasonality and daily weather conditions in relation to myocardial infarction and sudden cardiac death in Olmsted County, Minnesota, 1979 to 2002.
J Am Coll Cardiol. 2006 Jul 18;48(2):287-92. Epub 2006 Jun 22.

Sun Z.
Cardiovascular responses to cold exposure.
Front Biosci (Elite Ed). 2010 Jan 1;2:495-503.

Chen GF, Sun Z.
Effects of chronic cold exposure on the endothelin system.
J Appl Physiol. 2006 May;100(5):1719-26.

Abrignani MG, Corrao S, Biondo GB, Renda N, Braschi A, Novo G, Di Girolamo A, Braschi GB, Novo S.
Influence of climatic variables on acute myocardial infarction hospital admissions.
Int J Cardiol. 2009 Oct 2;137(2):123-9.

Goerre S, Egli C, Gerber S, Defila C, Minder C, Richner H, Meier B.
Impact of weather and climate on the incidence of acute coronary syndromes.
Int J Cardiol. 2007 May 16;118(1):36-40.

Bhaskaran K, Hajat S, Haines A, Herrett E, Wilkinson P, Smeeth L.
Effects of ambient temperature on the incidence of myocardial infarction.
Heart. 2009 Nov;95(21):1760-9.

Mercer JB.
Cold–an underrated risk factor for health.
Environ Res. 2003 May;92(1):8-13.

Murakami S, Otsuka K, Kono T, Soyama A, Umeda T, Yamamoto N, Morita H, Yamanaka G, Kitaura Y.
Impact of outdoor temperature on prewaking morning surge and nocturnal decline in blood pressure in a Japanese population.
Hypertens Res. 2011 Jan;34(1):70-3.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Blood Pressure and Vitamin C

healthy-fruitWhat Is High Blood Pressure?

Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps blood, and, if it stays elevated for a long time, can cause myriad health problems, including heart disease, stroke and kidney failure. Because it has no symptoms, it’s readily ignored. According to the CDC, about one third of Americans have elevated BP. If the first number is higher than 140 and the second is higher than 90, you have high blood pressure. If the first is 160 and the second is 100 or more, you are at stage 2 and really need intervention. It’s true that BP rises with age, but there still are things that can be, and should be, done about it.

There are factors you can control, and factors you can’t. Weight, too much salt, overdoing alcohol, insufficient potassium in the diet, sedentary lifestyle and smoking all are under your authority. Gender, race and family history aren’t. Despite the way it looks, stress can be managed, not always easily, but possible.

What Can I Do About It?

The DASH diet (Dietary Approaches to Stop Hypertension) focuses on very low sodium and high intake of fruits and vegetables, accompanied by a relatively low fat intake that includes lean meats, fish, and nuts and seeds. Being rich in fiber, nutrients and protein, the diet eliminates added sugars, added salt (you have to read labels), and sweets. Total salt consumption for the day shouldn’t exceed a teaspoonful. Because it’ll spike BP, alcohol is limited to two drinks a day for a man, one for a woman (McFarlane, 2007). Information about the DASH plan, either on paper or online, is available free at

We realize that the TV remote is a handy gadget. We also realize it put the kibosh on the last vestiges of physical activity for a slew of people. Before remotes were around, many of us used our kids to change channels. Not only high blood pressure, but also other health risks can be eliminated with a regimen of exercise. When you consider the options, exercise isn’t such a bad deal.

Most of us have a heart that is designed to pump blood a certain distance. Forcing it to pump harder and farther is akin to adding a hundred feet to the garden hose and watching it trickle for lack of water pressure. After a while, the heart gets tired of this slavery and goes on strike.  That’s when the trouble starts. Fat needs blood. Every extra pound of fat adds blood vessels.  The more than sixty thousand miles of tubes you already have doesn’t need to be enhanced by the extra miles that grow to feed fat. The bottom line? Lose weight and get your body mass index back where it belongs.

Inhaling a cigarette constricts blood vessels. That’s explains the light high that comes from the first smoke of the day. It reduces oxygen to the brain, just like booze, and you get a brief euphoria. But it can also make blood vessels stiff. Some say that smoking relieves stress.  Maybe so, but physical activity does the same thing and the effect lasts much longer. Plus, you can make new friends with exercise.

Do Supplements Help?

A recent report from Johns Hopkins University says that large doses of vitamin C can lower elevated blood pressure (Juraschek, 2012). The RDA for this vitamin is a mere 90 milligrams, barely enough to provide physiological benefit, but just enough to prevent scurvy. At 500 mg of vitamin C a day for at least eight weeks, subjects experienced a drop in systolic pressure of 3.8 mm Hg and a drop in diastolic pressure of 1.48 mm Hg. For those with existing high BP, the systolic drop was almost 5 mm Hg. Persons taking medication to control their BP could expect a 10 mm decrease. The lead author of this study, Edgar R. Miller, III, M.D., PhD, adds that, although the impact is moderate, it’s sufficient to decrease the number of stroke occurrences.  As is the case with any such investigation, additional study is warranted.

British scrutiny suggests that increased consumption of fruits and vegetables high in vitamin C is the way to go. This study indicated that people with high plasma values of the vitamin (from food) had lower clinical blood pressure. People who supplemented with vitamin C were excluded from this study, so one can only guess at the impact supplementation would have (Myint, 2011). Supplement users might be smiling at this point, or even smirking, but they need to know that combining vitamin C with certain other supplements might just undo what the vitamin can do. Lots of folks open several supplement bottles at one time without knowing of their interactions with each other, with foods, and with medications. This is not a prudent habit.  Many plant polyphenols are beneficial to human health. The timing of their ingestion is important. Australian researchers have found that combining vitamin C with grape seed polyphenols actually raises blood pressure. The hypothesis was that both substances, either alone or in combination, could lower elevated BP.  Vitamin C alone did. Polyphenols alone did not. The combo elevated BP by almost 5 points systolic and nearly 3 points diastolic (Ward, 2005). Need we advise caution and maybe a visit to a functional medicine dietitian or similarly-trained physician? Of course, this is only one study.

Beyond Vitamin C

Citrus fruits and their juices are among people’s favorites. A component of citrus called diosmin, also found in rosemary and used to address venous insufficiency, such as that in varicose veins and hemorrhoids, was found to be an anti-hypertensive agent in lab animals whose blood pressure was artificially elevated with a salt-laced compound. This flavonoid pigment was also found to rectify aberrant blood markers and to be protective of the heart and kidneys (Silambarasan, 2012).

Environmental Insults Raise Blood Pressure

Cadmium is one of the most important environmental pollutants that cause a number of adverse health effects. It’s a major component of tobacco smoke, emissions from steel and zinc production, waste incineration and coal combustion, and might be a fractional element of phosphate fertilizer manufacture (Hutton, 1983). Cadmium’s oxidative potential is witnessed in vascular dysfunction characterized by elevated arterial blood pressure and blunted response to vasoactive agents. Administration of ascorbic acid in a dose-dependent manner normalized blood pressure and improved vascular reactivity while suppressing the formation of oxidized substances (Donpunha, 2011). Lead exposure, whether chronic at low levels or acute at high levels, will elevate blood pressure in humans and animals. Like cadmium, it will generate free radicals and decrease available nitric oxide, the gas that relaxes blood vessels. Irani investigators found that vitamin C is able to prevent lead-induced hypertension (Mohammed, 2010).

Vitamins C is an anti-oxidant nutrient that seems to exert a healthful effect on blood pressure.  That does not leave room for self-treatment, however, because there is no definitive statement about eliminating the cause of hypertension or merely treating it as a symptom. Nonetheless, as adjunct to diet, exercise and lifestyle modification, it’s worth a try. But it isn’t without some pimples. It might reduce the response to warfarin and lower absorption, and might cause a false reading in some blood tests, as in a false increase in creatinine, a false increase in urinary calcium, and a false decrease in urinary sodium. Since vitamin C in large amounts is metabolized to oxalic acid, beware of kidney stones. On the other hand, if you smoke, you need high doses. In that case, get it from food.


Block G, Jensen CD, Norkus EP, Hudes M, Crawford PB.
Vitamin C in plasma is inversely related to blood pressure and change in blood pressure during the previous year in young Black and White women.
Nutr J. 2008 Dec 17;7:35

Chen J, He J, Hamm L, Batuman V, Whelton PK
Serum antioxidant vitamins and blood pressure in the United States population.
Hypertension. 2002 Dec;40(6):810-6.

Donpunha W, Kukongviriyapan U, Sompamit K, Pakdeechote P, Kukongviriyapan V, Pannangpetch P.
Protective effect of ascorbic acid on cadmium-induced hypertension and vascular dysfunction in mice.
Biometals. 2011 Feb;24(1):105-15.

Fernandes PR, Lira FA, Borba VV, Costa MJ, Trombeta IC, Santos Mdo S, Santos Ada C.
Vitamin C restores blood pressure and vasodilator response during mental stress in obese children.
[Article in English, Portuguese, Spanish]
Arq Bras Cardiol. 2011 Jun;96(6):490-7

He J, Wofford MR, Reynolds K, Chen J, Chen CS, Myers L, Minor DL, Elmer PJ, Jones DW, Whelton PK.
Effect of dietary protein supplementation on blood pressure: a randomized, controlled trial.
Circulation. 2011 Aug 2;124(5):589-95.

Hutton M.
Sources of cadmium in the environment.
Ecotoxicol Environ Saf. 1983 Feb;7(1):9-24.

Jalal DI, Smits G, Johnson RJ, Chonchol M
Increased fructose associates with elevated blood pressure.
J Am Soc Nephrol. 2010 Sep;21(9):1543-9.

Juraschek SP, Guallar E, Appel LJ, Miller ER 3rd.
Effects of vitamin C supplementation on blood pressure: a meta-analysis of randomized controlled trials.
Am J Clin Nutr. 2012 May;95(5):1079-88. Epub 2012 Apr 4.

McFarlane SI, von Gizycki H, Salifu M, Deshmukh M, Manieram M, Gebreegziabher Y, Gliwa AA, Bordia S, Shah S, Sowers JR.
Alcohol consumption and blood pressure in the adult US population: assessment of gender-related effects.
J Hypertens. 2007 May;25(5):965-70.

Mohammad A, Ali N, Reza B, Ali K.
Effect of ascorbic acid supplementation on nitric oxide metabolites and systolic blood pressure in rats exposed to lead.
Indian J Pharmacol. 2010 Apr;42(2):78-81.

Myint PK, Luben RN, Wareham NJ, Khaw KT.
Association between plasma vitamin C concentrations and blood pressure in the European prospective investigation into cancer-Norfolk population-based study.
Hypertension. 2011 Sep;58(3):372-9. Epub 2011 Jul 18.

Mullan BA, Young IS, Fee H, McCance DR.
Ascorbic acid reduces blood pressure and arterial stiffness in type 2 diabetes.
Hypertension. 2002 Dec;40(6):804-9.

Silambarasan T, Raja B.
Diosmin, a bioflavonoid reverses alterations in blood pressure, nitric oxide, lipid peroxides and antioxidant status in DOCA-salt induced hypertensive rats.
Eur J Pharmacol. 2012 Mar 15;679(1-3):81-9. Epub 2012 Jan 12.

Stamler J, Stamler R, Neaton JD.
Blood pressure, systolic and diastolic, and cardiovascular risks. US population data.
Arch Intern Med. 1993 Mar 8;153(5):598-615.

Teunissen-Beek KF, Dopheide J, Geleijnse JM, Bakker SJ, Brink EJ, de Leeuw PW, van Baak MA.
Protein supplementation lowers blood pressure in overweight adults: effect of dietary proteins on blood pressure (PROPRES), a randomized trial.
Am J Clin Nutr. 2012 Apr;95(4):966-71.

Vasdev S, Ford CA, Parai S, Longerich L, Gadag V.
Dietary vitamin C supplementation lowers blood pressure in spontaneously hypertensive rats.
Mol Cell Biochem. 2001 Feb;218(1-2):97-103.

Ward NC, Hodgson JM, Croft KD, Burke V, Beilin LJ, Puddey IB.
The combination of vitamin C and grape-seed polyphenols increases blood pressure: a randomized, double-blind, placebo-controlled trial.
J Hypertens. 2005 Feb;23(2):427-34.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Good News About Coffee

cup-of-coffee-on-saucerThe inveterate coffee drinkers among us will appreciate the good news about one of our favorite beverages. After all the flak we took about the vices of coffee, now’s the chance to respond. After water and tea, coffee is the next most popular drink on the planet, having a starring role in the history of several cultures. It came from the Muslim world, travelled to Italy and then to the rest of Europe, finally landing in the New World. At one time, it was limited only to religious observances.

The coffee bean is contained inside a “cherry” that grows on a small evergreen bush.  The Arabica strain is the more highly regarded of the two chief varieties, but the robusta strain is more resistant to the diseases peculiar to this plant, though less flavorful and more bitter. Arabica prefers the coolness of the mountainside; robusta will grow at lower elevations and in warmer climates. Since the best tasting coffee really is mountain grown, the sales talk of a particular brand is true. But Mrs. Olsen never told us that other brands also use mountain grown beans. She merely capitalized on a little-known fact.

One effect of coffee consumption is moderately elevated blood pressure, which is not surprising because caffeine is a stimulant. Italian studies done in the early 1990’s found that 200 milligrams of caffeine, about two cups’ worth, could raise systolic blood pressure by 10% and diastolic by 5% for up to two hours after consumption. The mechanism points to vasoconstriction (which has its own benefits), but researchers found no variation in heart rate or cardiac contractility (Casiglia, 1991), leading to an assumption that this temporary state is not a major concern, especially in light of later studies that reported no association between long-term coffee consumption and increase of cardiovascular complications (Mesas, 2011) or risk of hypertension (Geleijnse, 2008) (Klag, 2002).

Vitamin B6, known as pyridoxine, is a nutrient occasionally used to tame morning sickness in pregnancy and the throes of PMS. It’s also been used to address homocysteine imbalance, carpal tunnel syndrome, immunity deficiencies, and various behavioral/psychiatric issues. However, careless dosing of vitamin B6 can cause medical concerns that outweigh the benefits of producing the monoamine neurotransmitters, serotonin and dopamine. Large doses of B6 over a period of time can cause nerve fiber damage, particularly auditory neuropathy. You’d never think that coffee can prevent and treat this malady, but it does (Hong, 2008). One active coffee component is called trigonelline (Hong, 2009), an alkaloid also found in pumpkin that is able to modulate blood glucose (van Dijk, 2009) (Yoshinari, 2009). Because auditory neuropathy may be attenuated by trigonelline, why can’t the peripheral neuropathy of diabetes or physical trauma likewise be eased? It’s worth a look (Zhou, 2012).

Late-life dementia and Alzheimer’s disease (AD) are concerns shared by an aging population across the globe. Finnish studies followed a number of middle-agers for more than twenty years, documenting their coffee (and tea) consumption along the way.  Focusing more on caffeine than on coffee’s lesser-known constituents, researchers found that, over the long haul, those who drank three to five cups of coffee a day at midlife had a lower risk of dementia and AD in old age (Eskelinen, 2009, 2010).  American studies later found that long-term coffee consumption protects against cognitive impairment by reducing the formation of amyloid beta, the protein that forms the plaques associated with AD. Here it was inferred that caffeine is part of a synergy that affords the desired effect, with many coffee constituents not yet identified (Cao, 2011).

Because early research had indicated that coffee may be protective against conditions other than neurological, scientists took the trigonelline link a little further. It’s accepted that people with diabetes are at risk for cognitive dysfunction. Initially, it was proposed that coffee was merely to be explored as a tool in the management of diabetes and related sequelae (Biessels, 2010). It was realized, however, that caffeine can decrease the risk of type 2 diabetes and consequent cognitive decline (Salazar-Martinez, 2004) (Tuomilehto, 2004).

In general, coffee increases plasma antioxidant capacity, possibly because of the contribution, bioavailability and activity of its particular group of polyphenols, including chlorogenic acid, one component linked to a reduction of type 2 diabetes risk by virtue of delaying intestinal glucose absorption and the inhibition of gluconeogenesis (Ong, 2010) (Tunnicliffe, 2011). Other medical conditions are purported to be influenced by coffee’s mechanisms, including gastrointestinal diseases (Inoue, 1998), gallstones (Leitzmann, 1999), and Parkinson’s disease (Checkoway, 2002) (Blanchette, 2000).

If coffee has a down side, it’s that it can interact with some drugs, most notably quinolone antibiotics, such as ciprofloxacin and its kin, which increase caffeine concentrations by inhibiting its clearance (Harder, 1989). Coffee’s popularity cannot be ignored. Just look at all the coffee options that run the gamut from hot to cold, from sweet to sweeter, and from low-cal to mega-cal. Since the 1989 expiration of a global agreement to stabilize supply, availability has fluctuated—and so has the price. You can’t even get the cup for a dime any more.


Biessels GJ.
Caffeine, diabetes, cognition, and dementia.
J Alzheimers Dis. 2010;20 Suppl 1:S143-50.

Campdelacreu J.
Parkinson disease and Alzheimer disease: environmental risk factors.
[Article in English, Spanish]

Neurologia. 2012 Jun 13. [Epub ahead of print]

Cao C, Wang L, Lin X, Mamcarz M, Zhang C, Bai G, Nong J, Sussman S, Arendash G.
Caffeine synergizes with another coffee component to increase plasma GCSF: linkage to cognitive benefits in Alzheimer’s mice.
J Alzheimers Dis. 2011;25(2):323-35.

Casiglia E, Bongiovì S, Paleari CD, Petucco S, Boni M, Colangeli G, Penzo M, Pessina AC.
Haemodynamic effects of coffee and caffeine in normal volunteers: a placebo-controlled clinical study.
J Intern Med. 1991 Jun;229(6):501-4.

Checkoway H, Powers K, Smith-Weller T, Franklin GM, Longstreth WT Jr, Swanson PD.
Parkinson’s disease risks associated with cigarette smoking, alcohol consumption, and caffeine intake.
Am J Epidemiol. 2002 Apr 15;155(8):732-8.

Eskelinen MH, Ngandu T, Tuomilehto J, Soininen H, Kivipelto M.
Midlife coffee and tea drinking and the risk of late-life dementia: a population-based CAIDE study.
J Alzheimers Dis. 2009;16(1):85-91.

Eskelinen MH, Kivipelto M.
Caffeine as a protective factor in dementia and Alzheimer’s disease.
J Alzheimers Dis. 2010;20 Suppl 1:S167-74.

Floegel A, Pischon T, Bergmann MM, Teucher B, Kaaks R, Boeing H
Coffee consumption and risk of chronic disease in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Germany study.
Am J Clin Nutr. 2012 Apr;95(4):901-8.

Yoichi Fukushima, Takashi Ohie, Yasuhiko Yonekawa, Kohei Yonemoto, Hiroki Aizawa, Yoko Mori, Makoto Watanabe, Masato Takeuchi, Maiko Hasegawa, Chie Taguchi and Kazuo Kondo
Coffee and Green Tea As a Large Source of Antioxidant Polyphenols in the Japanese Population
Journal of Agricultural and Food Chemistry 2009 57 (4), 1253-1259

Gelber RP, Petrovitch H, Masaki KH, Ross GW, White LR.
Coffee intake in midlife and risk of dementia and its neuropathologic correlates.
J Alzheimers Dis. 2011;23(4):607-15.

Geleijnse JM.
Habitual coffee consumption and blood pressure: an epidemiological perspective.
Vasc Health Risk Manag. 2008;4(5):963-70.

Harder S, Fuhr U, Staib AH, Wolff T.
Ciprofloxacin-caffeine: a drug interaction established using in vivo and in vitro investigations.
Am J Med. 1989 Nov 30;87(5A):89S-91S.

Head KA.
Peripheral neuropathy: pathogenic mechanisms and alternative therapies.
Altern Med Rev. 2006 Dec;11(4):294-329.

Hermansen K, Krogholm KS, Bech BH, Dragsted LO, Hyldstrup L, Jørgensen K, Larsen ML, Tjønneland AM.
Coffee can protect against disease
Ugeskr Laeger. 2012 Sep 24;174(39):2293-2297.

Hong BN, Yi TH, Park R, Kim SY, Kang TH.
Coffee improves auditory neuropathy in diabetic mice.
Neurosci Lett. 2008 Aug 29;441(3):302-6. Epub 2008 Jun 22.

Hong BN, Yi TH, Kim SY, Kang TH.
High-dosage pyridoxine-induced auditory neuropathy and protection with coffee in mice.
Biol Pharm Bull. 2009 Apr;32(4):597-603.

Huxley R, Lee CM, Barzi F, Timmermeister L, Czernichow S, Perkovic V, Grobbee DE, Batty D, Woodward M.
Coffee, decaffeinated coffee, and tea consumption in relation to incident type 2 diabetes mellitus: a systematic review with meta-analysis.
Arch Intern Med. 2009 Dec 14;169(22):2053-63.

Inoue M, Tajima K, Hirose K, Hamajima N, Takezaki T, Kuroishi T, Tominaga S.
Tea and coffee consumption and the risk of digestive tract cancers: data from a comparative case-referent study in Japan.
Cancer Causes Control. 1998 Mar;9(2):209-16.

Kaiser permanante Division of Research
Coffee Drinking and Caffeine Associated with Reduced Risk of Hospitalization for Heart Rhythm Disturbances

Klag MJ, Wang NY, Meoni LA, Brancati FL, Cooper LA, Liang KY, Young JH, Ford DE.
Coffee intake and risk of hypertension: the Johns Hopkins precursors study.
Arch Intern Med. 2002 Mar 25;162(6):657-62.

Leitzmann MF, Willett WC, Rimm EB, Stampfer MJ, Spiegelman D, Colditz GA, Giovannucci E.
A prospective study of coffee consumption and the risk of symptomatic gallstone disease in men.
JAMA. 1999 Jun 9;281(22):2106-12.

Mesas AE, Leon-Muñoz LM, Rodriguez-Artalejo F, Lopez-Garcia E.
The effect of coffee on blood pressure and cardiovascular disease in hypertensive individuals: a systematic review and meta-analysis.
Am J Clin Nutr. 2011 Oct;94(4):1113-26. Epub 2011 Aug 31.

Oba S, Nagata C, Nakamura K, Fujii K, Kawachi T, Takatsuka N, Shimizu H.
Consumption of coffee, green tea, oolong tea, black tea, chocolate snacks and the caffeine content in relation to risk of diabetes in Japanese men and women.
Br J Nutr. 2010 Feb;103(3):453-9. Epub 2009 Oct 12.

Ong KW, Hsu A, Tan BK.
Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes.
PLoS One. 2012;7(3):e32718. Epub 2012 Mar 7.

Richelle M, Tavazzi I, Offord E.
Comparison of the antioxidant activity of commonly consumed polyphenolic beverages (coffee, cocoa, and tea) prepared per cup serving.
J Agric Food Chem. 2001 Jul;49(7):3438-42.

Ross GW, Abbott RD, Petrovitch H, Morens DM, Grandinetti A, Tung KH, Tanner CM, Masaki KH, Blanchette PL, Curb JD, Popper JS, White LR.
Association of coffee and caffeine intake with the risk of Parkinson disease.
JAMA. 2000 May 24-31;283(20):2674-9.

Salazar-Martinez E, Willett WC, Ascherio A, Manson JE, Leitzmann MF, Stampfer MJ, Hu FB.
Coffee consumption and risk for type 2 diabetes mellitus.
Ann Intern Med. 2004 Jan 6;140(1):1-8.

Tunnicliffe JM, Eller LK, Reimer RA, Hittel DS, Shearer J.
Chlorogenic acid differentially affects postprandial glucose and glucose-dependent insulinotropic polypeptide response in rats.
Appl Physiol Nutr Metab. 2011 Oct;36(5):650-9. Epub 2011 Oct 6.

Tuomilehto J, Hu G, Bidel S, Lindström J, Jousilahti P.
Coffee consumption and risk of type 2 diabetes mellitus among middle-aged Finnish men and women.
JAMA. 2004 Mar 10;291(10):1213-9.

van Dijk AE, Olthof MR, Meeuse JC, Seebus E, Heine RJ, van Dam RM.
Acute effects of decaffeinated coffee and the major coffee components chlorogenic acid and trigonelline on glucose tolerance.
Diabetes Care. 2009 Jun;32(6):1023-5. Epub 2009 Mar 26.

Yoshinari O, Sato H, Igarashi K.
Anti-diabetic effects of pumpkin and its components, trigonelline and nicotinic acid, on Goto-Kakizaki rats.
Biosci Biotechnol Biochem. 2009 May;73(5):1033-41. Epub 2009 May 7.

Zhou J, Chan L, Zhou S.
Trigonelline: a plant alkaloid with therapeutic potential for diabetes and central nervous system disease.
Curr Med Chem. 2012 Jul 1;19(21):3523-31.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Importance of Healthy Kidneys

kidney-modelBert Lance, who worked for Jimmy Carter in the Budget office, is credited with saying, “If it ain’t broke, don’t fix it,” as cited in the May 1977 issue of the magazine Nation’s Business. Sometimes we carry this admonition too far, as when we ignore body parts that don’t hurt. Not everything that’s out of order lets us know right away. It’s a lot easier to prevent damage than to fix it; just as changing the oil in your car prevents an exorbitant repair bill. The same applies to your body. Preventing ailments is easier and less painful than fixing them. Except for stones, the kidneys pretty much mind their own business, seldom letting us know they’re even there. A little maintenance goes a long way. Many people don’t even know where in the body they are or what they do.

These bean-shaped organs, about the size of a fist, are near the middle of the back, just below the ribs, one on each side of the spine. And, boy oh boy, are they sophisticated reprocessing machines. They handle nearly fifty gallons of blood a day to filter about a half gallon of waste and excess water, which you already know is stored in the bladder. The wastes come from food leftovers that float in the blood after the food’s energy supplies have been used. If these wastes weren’t removed, they’d make us sick. The actual removal of the impurities occurs in the nephrons, which are the functional units of the kidney. Each kidney has more than a million nephrons, which have tiny blood vessels that help to remove the junk, including urea, uric acid, creatinine from muscles, and excess electrolytes. Normal proteins and other materials are kept in the bloodstream to be recycled for use by the body. This includes potassium, phosphorus and sodium, among others. The kidneys also release three vital hormones—erythropoietin to stimulate the marrow to make red blood cells, renin to control blood pressure, and calcitriol (the active form of vitamin D) to help maintain calcium for bones.

If kidney function were to fail by as much as thirty percent, you probably wouldn’t even know it. That’s one of the reasons why it’s measured on blood tests, looking at creatinine, glomerular filtration rate (GFR) and blood urea nitrogen (BUN). The first of these comes from normal wear and tear on muscles; the second is an age-variable measure of how well the kidneys filter the wastes; and the third is a product of protein breakdown from the foods you eat. Proteins can also be monitored via urine. It is possible to survive with only one kidney, but living with two is nicer. If function drops to fifteen percent, either dialysis or a transplant may be necessary to sustain life.

There are things we can do to prevent kidney disorders. If there is a family history of diabetes or high blood pressure, tend to those right away. Glucose that stays in the blood instead of getting used for fuel can damage the nephrons. High BP distresses the tiny blood vessels of the nephrons, interfering with their function. Yes, there are medications to address these problems, but there also are a few dietary interventions that can keep the kidneys healthy.

Keeping sodium under control is necessary, especially as we age. Processed meals and meats contain large amounts of sodium, but so do restaurant foods, fast foods, soups and snacks. In some who are susceptible, sodium may spike BP.

The same oxygen that gives us life takes away molecular stability in the form of free radicals, which take turns stealing electrons from each other in a continuous cycle. Some come from the environment as pollution, and some from inside the body from burning food for energy. Supplying both the fat-soluble and water-soluble anti-oxidants from supplements is a good start, but that does not rule out the importance of the right diet, from which you can make the master anti-oxidant, glutathione.

Too much protein can tax the kidneys, particularly animal proteins. Mixing plant and animal sources is a safe bet. Whole grains and legumes can help. Depending on the condition of the body, however, protein intake in excess of protein need may or may not adversely affect the kidneys (Martin, 2005) (Knight, 2003). In the presence of a jeopardized kidney, elevated phosphorus levels can do harm. Meats and dairy are main sources, but food additives also contribute to the load. Phosphorus is an essential element in the diet, and in the form of phosphates is a major component of bone. It’s necessary for the manufacture of adenosine triphosphate to be burned for energy. Without it, metabolism of calcium, protein and glucose is upset. But an excess burdens the filtration load of the nephrons, and phosphate retention is linked to parathyroid malfunction.

Now, what do we eat?  Reducing sodium intake is simple. Just do it. More than 500 mg at a meal is pushing it, so you have to read labels. Canned soups can give you half a day’s worth in a single serving. You can swallow anti-oxidants from a bottle, but it’s helpful to get some from food. Berries are an excellent source, as are peppers, squashes and tomatoes. Cruciferous vegetables supply vitamin C, while onions offer quercetin, an anti-oxidant bioflavonoid that is also cardio-protective. Apples, with skins, are anti-inflammatory. Egg whites are a source of complete protein, having all the essential amino acids and less than a dozen milligrams of phosphorus. The omega-3 fats from cold-water fish—and from fish oil—can’t be beat for anti-inflammatory work (see and olive oil is rich in polyphenols that inhibit inflammation and oxidation. A reliable research link for the study of kidney health is DaVita Clinical Research,

Water is an essential nutrient. Though we think that more is better, the truth is that more can be toxic. Drink too much and the kidneys can’t keep up. The cells get swollen beyond their capacity, sodium levels drop precipitously, and the firing of neurotransmitters short circuits, leading to headaches, fatigue, disorientation and even death. Thinking water will reduce protein blood test values, some people will overdo water intake and find that all they have done is dilute the protein. Even endurance athletes need to balance water intake with water loss.

A little prevention costs less than a plumber.


Berner YN, Shike M.
Consequences of phosphate imbalance.
Annu Rev Nutr. 1988;8:121-48.

Birn H.
The kidney in vitamin B12 and folate homeostasis: characterization of receptors for tubular uptake of vitamins and carrier proteins.
Am J Physiol Renal Physiol. 2006 Jul;291(1):F22-36.

Jane Chiu, M.Sc., Zia A. Khan, Ph.D., Hana Farhangkhoee, M.Sc., Subrata Chakrabarti, M.D., Ph.D
Curcumin prevents diabetes-associated abnormalities in the kidneys by inhibiting p300 and nuclear factor-κB
Nutrition. Volume 25, Issue 9 , Pages 964-972, September 2009

D’Amico G, Gentile MG.
Effect of dietary manipulation on the lipid abnormalities and urinary protein loss in nephrotic patients.
Miner Electrolyte Metab. 1992;18(2-5):203-6.

Duffield JS, Hong S, Vaidya VS, Lu Y, Fredman G, Serhan CN, Bonventre JV.
Resolvin D series and protectin D1 mitigate acute kidney injury.
J Immunol. 2006 Nov 1;177(9):5902-11.

Gentile MG, Fellin G, Cofano F, Delle Fave A, Manna G, Ciceri R, Petrini C, Lavarda F, Pozzi F, D’Amico G.
Treatment of proteinuric patients with a vegetarian soy diet and fish oil.
Clin Nephrol. 1993 Dec;40(6):315-20.

Kalista-Richards M.
The kidney: medical nutrition therapy–yesterday and today.
Nutr Clin Pract. 2011 Apr;26(2):143-50. doi: 10.1177/0884533611399923.

Knight EL, Stampfer MJ, Hankinson SE, Spiegelman D, Curhan GC.
The impact of protein intake on renal function decline in women with normal renal function or mild renal insufficiency.
Ann Intern Med. 2003 Mar 18;138(6):460-7.

Martin WF, Armstrong LE, Rodriguez NR.
Dietary protein intake and renal function.
Nutr Metab (Lond). 2005 Sep 20;2:25.

Ogborn MR, Nitschmann E, Bankovic-Calic N, Weiler HA, Aukema HM.
Dietary soy protein benefit in experimental kidney disease is preserved after isoflavone depletion of diet.
Exp Biol Med (Maywood). 2010 Nov;235(11):1315-20. doi: 10.1258/ebm.2010.010059. Epub 2010 Oct 4.

Rayner TE, Howe PR.
Purified omega-3 fatty acids retard the development of proteinuria in salt-loaded hypertensive rats.
J Hypertens. 1995 Jul;13(7):771-80.

Soroka N, Silverberg DS, Greemland M, Birk Y, Blum M, Peer G, Iaina A.
Comparison of a vegetable-based (soya) and an animal-based low-protein diet in predialysis chronic renal failure patients.
Nephron. 1998;79(2):173-80.

National Kidney Disease Education Program

Tack, Ivan MD, PhD
Effects of Water Consumption on Kidney Function and Excretion
Nutrition Today: November/December 2010 – Volume 45 – Issue 6 – pp S37-S40

Zararsiz I, Sonmez MF, Yilmaz HR, Tas U, Kus I, Kavakli A, Sarsilmaz M.
Effects of omega-3 essential fatty acids against formaldehyde-induced nephropathy in rats.
Toxicol Ind Health. 2006 Jun;22(5):223-9.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Mineral Balance: Sodium-Potassium

sodium-potassium-scaleLike children on a see-saw, some minerals work to balance each other in the body. Almost everything in nature is about balance. In humans and animals it’s called homeostasis, which is the property of the body to maintain its internal environment in a stable, constant condition. Occasionally, mainstream medicine overlooks the balance aspect and tends to look at isolated parts and actions of the body. One of these oversights involves sodium and its relationship with potassium, working together as the sodium-potassium pump, which is the mechanism of active transport by which sodium and potassium ions are moved across the cell membrane, into and out of the cell. With the help of ATP as the source of energy, sodium is extruded from the cell and potassium is invited in. This energetic display is necessary for protein biosynthesis, maintenance of osmotic equilibrium, initiation of nerve impulses and transport of some other molecules, such as glucose, across the membrane. To clarify, ATP is a high-energy phosphate compound used by the body to get things done, including muscle contractions and enzyme metabolism, among others.

Sodium (Na) and potassium (K) are essential minerals and electrolytes. As the latter, they dissociate into ions (charged particles), allowing them to conduct electricity. In order for the body to function the right way, they need to be regulated on both sides of the cell membrane. The recommended intake of sodium had been 2300 milligrams a day, but is now 1500 mg/d; that for potassium being unchanged at 4700 mg/day. The sodium:potassium ratio, therefore, has moved from 1:2 to almost 1:3, which is closer to what is believed to be the body’s ideal. In plants, of which humans eat too few, the natural ratio of Na to K is about 1:10.

Sodium is the chief ion outside the cell, potassium inside. Inside the cell, sodium concentrations are ten times lower than outside. Potassium concentration inside are about thirty times higher than outside. The difference across the membrane creates an electrochemical gradient known as membrane potential, which uses a lot of the body’s energy to maintain itself. Without this tight control, muscles would suffer, especially the heart. In the typical American diet, intake of sodium (as sodium chloride) is three times higher than potassium, just the opposite of what it should be. The dietary guidelines for sodium consumption are currently being met by only a tiny percent of the population (Drewnowski, 2012)

Table salt is about 39% sodium. A simple explanation is that one teaspoon of salt, which has a mass about 6200 mg, contains approximately 2400 mg of sodium.

The National Health and Nutrition Examination Survey (NHANES), first conducted in the early 70’s, reported in 2012 that more than 90% of adults consumed more than 2300 mg/d of sodium a day, and less than 2%–that’s two percent—met the recommendation for potassium (Cogswell, 2012). It’s no small surprise that high blood pressure is rampant (Wenberger, 1986) (Elliot, 1991, 1996) (Dyer, 1995) (He, 2004) (Levings, 2012)  Of course, you could argue that the relationship of sodium intake to hypertension is a genetic matter, but do you know your genes?

Increasing potassium and reducing sodium intake will help to reduce blood pressure. But be careful not to overdo it by using supplements without strict supervision, since potassium overload is almost as bad as potassium deficiency. After all, potassium is used to stop the heart in lethal injections. Aiming for the recommended 4700 mg a day means that vegetables and fruit intake needs to go up, while intake of cakes, cookies and prepared foods needs to go down. Overdosing potassium from foods is almost impossible…you can’t eat that much food.

If less than 2% of Americans get the recommended amount of potassium, how much do we get?  From data collected in 2009-2010, women get about 50% of the RDI, men about 81% (USDA, 2012). Besides supporting coronary health, potassium seems to lower the risk of stroke (Ascherio, 1998) (Larsson, 2011). If you’ve got abnormally high urinary calcium levels, you might be looking at kidney stones in your future, something we wouldn’t wish on anyone.  Increasing dietary potassium levels by increasing fruit and vegetable intake has been found to decrease urinary calcium excretion. Taking a supplement under supervision will do the same thing. It has been found that getting more than 4000 mg of potassium a day reduces risk of kidney stones (Curhan, 2004).

Diuretics may lower potassium levels, but not all do, so check with your doctor to find out if your diuretic is potassium-sparing or not. Laxatives, caffeine, tobacco and lots of sugar may also compromise potassium stores. Physical and mental stress interferes with potassium metabolism. If you haven’t already, try to increase potassium foods, including sweet potatoes, bananas, tomatoes, oranges, beans, squashes, nuts and seeds, green foods, avocados, garlic and a host of other produce. Look here for a list:

Look at both sodium and potassium in the context of what you eat every day and try to balance foods before you consider a potassium supplement. You know where most of the salt comes from (processed foods and the salt shaker), but you’ll have to read labels to find the rest. If you can maintain a ratio of one to one, you’ll be better off than most, but trying to get two to one, potassium to sodium, is preferred. Limiting sodium to about 500 mg in a meal is a virtuous endeavor. Look at some soup cans and you’ll see more than that in a tiny serving’s worth.  Even certain “light” soups have 650 mg of sodium in a 1-cup serving. Potassium values of these products are half that, which is the opposite of what it should be.  If the whole can is consumed, sodium-potassium balance needs to be addressed at other meals. Seeing kids unbalanced on a see-saw can be amusing. Viewing sodium-potassium balance from a gurney is not.


Arcand J, Steckham K, Tzianetas R, L’Abbe MR, Newton GE.
Evaluation of Sodium Levels in Hospital Patient Menus
Arch Intern Med. 2012;172(16):1261-1262.

Ascherio A, Rimm EB, Hernán MA, Giovannucci EL, Kawachi I, Stampfer MJ, Willett WC.
Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men.
Circulation. 1998 Sep 22;98(12):1198-204.

Barri YM, Wingo CS.
The effects of potassium depletion and supplementation on blood pressure: a clinical review.
Am J Med Sci. 1997 Jul;314(1):37-40.

Centers for Disease Control and Prevention (CDC).
Usual sodium intakes compared with current dietary guidelines — United States, 2005-2008.
MMWR Morb Mortal Wkly Rep. 2011 Oct 21;60(41):1413-7.

Cogswell ME, Zhang Z, Carriquiry AL, Gunn JP, Kuklina EV, Saydah SH, Yang Q, Moshfegh AJ.
Sodium and potassium intakes among US adults: NHANES 2003-2008.
Am J Clin Nutr. 2012 Sep;96(3):647-57.

Curhan GC, Willett WC, Knight EL, Stampfer MJ.
Dietary factors and the risk of incident kidney stones in younger women: Nurses’ Health Study II.
Arch Intern Med. 2004 Apr 26;164(8):885-91.

Denton D, Weisinger R, Mundy NI, Wickings EJ, Dixson A, Moisson P, Pingard AM, Shade R, Carey D, Ardaillou R, et al.
The effect of increased salt intake on blood pressure of chimpanzees.
Nat Med. 1995 Oct;1(10):1009-16.

Drewnowski A, Maillot M, Rehm C.
Reducing the sodium-potassium ratio in the US diet: a challenge for public health.
Am J Clin Nutr. 2012 Aug;96(2):439-44.

Dyer AR, Stamler R, Elliott P, Stamler J.
Dietary salt and blood pressure.
Nat Med. 1995 Oct;1(10):994-6.

Elliott P
Observational studies of salt and blood pressure.
Hypertension. 1991 Jan;17(1 Suppl):I3-8.

Elliott P, Stamler J, Nichols R, Dyer AR, Stamler R, Kesteloot H, Marmot M.
Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations. Intersalt Cooperative Research Group.
BMJ. 1996 May 18;312(7041):1249-53.

He FJ, MacGregor GA.
Effect of longer-term modest salt reduction on blood pressure.
Cochrane Database Syst Rev. 2004;(3):CD004937

Hoorn EJ, Betjes MG, Weigel J, Zietse R.
Hypernatraemia in critically ill patients: too little wat
er and too much salt.

Nephrol Dial Transplant. 2008 May;23(5):1562-8.

Krishna GG, Chusid P, Hoeldtke RD.
Mild potassium depletion provokes renal sodium retention.
J Lab Clin Med. 1987 Jun;109(6):724-30.

Krishna GG.
Role of potassium in the pathogenesis of hypertension.
Am J Med Sci. 1994 Feb;307 Suppl 1:S21-5.

Larsson SC, Virtamo J, Wolk A.
Potassium, calcium, and magnesium intakes and risk of stroke in women.
Am J Epidemiol. 2011 Jul 1;174(1):35-43.

Levings J, Cogswell M, Curtis CJ, Gunn J, Neiman A, Angell SY.
Progress toward sodium reduction in the United States.
Rev Panam Salud Publica. 2012 Oct;32(4):301-6.

National Institute of Health
Jan. 26, 2009
Sodium/Potassium Ratio Linked to Cardiovascular Disease Risk

Akira Okayama; Katsuyuki Miura; Tomonori Okamura; Nagako Okuda; Shigeyuki Saitoh; et al
Abstract MP077: Dietary Sodium Potassium Ratio as a Risk Factor for Stroke, Cardiovascular Diseases and All-cause Death Among Japanese: Nippondata80.
Circulation. 2012; 125: AMP077

Quanhe Yang, PhD; Tiebin Liu, MSPH; Elena V. Kuklina, MD, PhD; et al.
Sodium and Potassium Intake and Mortality Among US AdultsProspective Data From the Third National Health and Nutrition Examination Survey FREE
Arch Intern Med. 2011;171(13):1183-1191.

Lynn D. Silver, MD, MPH; Thomas A. Farley, MD, MPH
Sodium and Potassium Intake: Mortality Effects and Policy ImplicationsComment on “Sodium and Potassium Intake and Mortality Among US Adults”
Arch Intern Med. 2011;171(13):1191-1192.

Stofan JR, Zachwieja JJ, Horswill CA, Murray R, Anderson SA, Eichner E
Sweat and sodium losses in NCAA football players: a precursor to heat cramps?
Int J Sport Nutr Exerc Metab. 2005 Dec;15(6):641-52.

U.S. Department of Agriculture, Agricultural Research Service. 2012.
Total Nutrient Intakes: Percent Reporting and Mean Amounts of Selected Vitamins and Minerals from Food and Dietary
Supplements, by Family Income (as ! of Federal Poverty Threshold) and Age, What We Eat in America, NHANES 2009-2010. Available:
USDA, Agricultural Research Services

Dietary Guidelines for Americans 2005
Appendix B-1. Food Sources of Potassium

USDA. Downloadable pdf Tables.
What We Eat in America, 2009-2010.

Weinberger MH, Miller JZ, Luft FC, Grim CE, Fineberg NS.
Definitions and characteristics of sodium sensitivity and blood pressure resistance.
Hypertension. 1986 Jun;8(6 Pt 2):II127-34.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Hypertension and The Kidneys

HypertensionFor their size, the kidneys do an awful lot of work. Besides filtering the blood of potentially harmful substances, they secrete hormones that influence the manufacture of red blood cells and the absorption and metabolism of calcium. Another job is to monitor blood pressure and to take corrective action if it drops. The kidney does this by secreting a proteolytic enzyme called renin (not to be confused with rennin, the bovine enzyme that curdles milk and is used to make cheeses and junkets), whose function is to control another hormone, angiotensin, the polypeptide that constricts blood vessels. Angiotensin, especially angiotensin 2, is occasionally the target of blood pressure medications. This compound constricts the walls of arterioles and closes capillary beds, causing the kidney to reabsorb sodium while stimulating the adrenal cortex to release aldosterone, itself encouraging the kidney to reclaim still more sodium and, therefore, water. To add to this complicated cycle, angiotensin 2 prompts the pituitary to secrete vasopressin, yet another hormone that constricts blood vessels and elevates blood pressure, but also reduces excretion of urine by causing the kidney to reabsorb water. Because of this activity, vasopressin is also known as antidiuretic hormone, which conserves water stores in times of dehydration. All this spirited activity is directed by the brain.

We all realize that blood pressure (BP) involves the heart. In response to elevated BP, the heart releases two natriuretic peptides, type A and type B. (natri from ‘sodium’ and uretic from urine). These hormones relax the arterioles, inhibit the secretion of renin and aldosterone, and constrain the reabsorption of sodium ions by the kidney. This reduces reabsorption of water, so the volume of urine increases along with the volume of sodium in it. The net effect is to lower BP by reducing the volume of blood in the circulatory system. Whew! If ever you have heard the expression from Psalm 139:14 that mentions man being fearfully and wonderfully made, you now know what it means.

High blood pressure, usually anything above 140/90, can be caused by a number of things, including overweight, race, age, diet and exercise, family history, smoking, alcohol and stress levels. Healthy lifestyle can help. If there is such a thing as a worldwide hypertension epidemic, it may now be addressed by tackling a newfound cellular source in the brain, the targeting of which can reverse the condition. It has been found that angiotensin 2 is causative of hypertension because of the dysregulation of certain brain mechanisms involving the endoplasmic reticulum (Young, 2012).

The Endo What?
The endoplasmic reticulum is common to all eukaryotic cells—those that have a membrane-bound nucleus, genetic material organized within chromosomes, and organelles, such as mitochondria, chloroplasts…and endoplasmic reticula (ER). The ER is a network of membranes important to protein synthesis and folding, and it helps in the transport of cellular materials. The actual job of the ER varies from cell type to cell type, and occasionally within the same cell, depending on whether it is smooth or rough. The smooth ER is shaped like a tube and synthesizes phospholipids, which are the chief constituents of cell membranes. It also breaks down toxins in the liver, helps to regulate calcium concentrations, and controls the metabolism of carbohydrates. The rough ER is a line of flattened sacs with little bumps called ribosomes on the outside. This is where serum proteins, such as albumin, are synthesized.

Back To BP
Researchers have recently found that a water-soluble (hydrophilic) bile acid called tauroursodeoxycholic acid (TUDCA) reduces stress to the endoplasmic reticulum, which acts as a stress manager for every cell. If something goes wrong in a cell, the ER starts processes that help adapt to the stressors, angiotensin 2 among them. Because different ER’s do different jobs, only those that orchestrate the cascade of events causing hypertension are influenced by TUDCA. These are located outside the blood-brain barrier, near the bottom, allowing them to be affected by substances that are too large to cross the barrier, such as certain medications. Nonetheless, these ER’s are able to communicate with the brain’s inner chambers. TUDCA may then be able to treat the stress on hypertension-related endoplasmic reticula that control the release of angiotensin 2 (Young, 2012).

Chronic metabolic disorders, such as obesity, diabetes and insulin resistance are also mediated by the ER’s failure or success in launching an adequate stress defense.  Insulin resistance associated with the production of inflammatory factors, both related to fat cells, can activate the ER stress pathway. Research at the Hallet Diabetes Center of Brown University discovered that TUDCA reduces inflammatory signaling and thus may attenuate the ER stressors that trigger blood pressure elevation (Jiao, 2011). Additional study of intracellular regulatory proteins found that regular treatment with TUDCA lowers systolic blood pressure while lessening glucose intolerance (Ceylan-Isik, 2011).

Overactivity of the renin-angiotensin system, for which the kidneys are partly responsible, leads to the vasoconstriction that characterizes hypertension. It is easier to control angiotensin than renin, so angiotensin-related drugs are used, such as ACE inhibitors or angiotensin-receptor blockers (ARBs). It is renin that converts angiotensin. Renin blockers demonstrate poor bioavailability, so are rarely used. To avoid the side effects that accompany drugs, sodium reduction is the first step of a natural protocol in giving the kidneys a break and reducing BP. Following the DASH diet (Dietary Approaches to Stop Hypertension) is not a difficult strategy (Sacks, 2001) (Svetkey, 1999). Water will clear wastes from the kidneys, acidulation being recommended. Increase vegetable intake while reducing meat, especially red. Fill half the plate or more with produce. To bless the kidneys and to control BP add omega-3 fatty acids to the daily regimen (Friedman, 2010) (Cabo 2012) (Mori, 2010). If urine is any darker than a manila folder, drink more water.


Amin A, Choi SK, Galan M, Kassan M, Partyka M, Kadowitz P, Henrion D, Trebak M, Belmadani S, Matrougui K.
Chronic inhibition of endoplasmic reticulum stress and inflammation prevents ischaemia-induced vascular pathology in type II diabetic mice.
J Pathol. 2012 Jun;227(2):165-74.

Aneja A, El-Atat F, McFarlane SI, Sowers JR.
Hypertension and obesity.
Recent Prog Horm Res. 2004;59:169-205.

Cabo J, Alonso R, Mata P.
Omega-3 fatty acids and blood pressure
Br J Nutr. 2012 Jun;107 Suppl 2:S195-200.

Ceylan-Isik AF, Sreejayan N, Ren J.
Endoplasmic reticulum chaperon tauroursodeoxycholic acid alleviates obesity-induced myocardial contractile dysfunction.
J Mol Cell Cardiol. 2011 Jan;50(1):107-16.

Colin N. Young, Xian Cao, Mallikarjuna R. Guruju, Joseph P. Pierce, Donald A. Morgan, Gang Wang, Costantino Iadecola, Allyn L. Mark, Robin L. Davisson
ER stress in the brain subfornical organ mediates angiotensin-dependent hypertension
J Clin Inv. November 1, 2012; Volume 122, issue 11: 3960

Esler M, Jennings G, Biviano B, Lambert G, Hasking G.
Mechanism of elevated plasma noradrenaline in the course of essential hypertension.
J Cardiovasc Pharmacol. 1986;8 Suppl 5:S39-43.

Esler M.
High blood pressure management: potential benefits of I1 agents.
J Hypertens Suppl. 1998 Aug;16(3):S19-24.

Esler M, Kaye D.
Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease.
J Cardiovasc Pharmacol. 2000;35(7 Suppl 4):S1-7.

Friedman AN.
Omega-3 fatty acid supplementation in advanced kidney disease.
Semin Dial. 2010 Jul-Aug;23(4):396-400.

Hall JE, Brands MW, Henegar JR.
Mechanisms of hypertension and kidney disease in obesity.
Ann N Y Acad Sci. 1999 Nov 18;892:91-107.

Hall JE.
The kidney, hypertension, and obesity.
Hypertension. 2003 Mar;41(3 Pt 2):625-33.

Hotamisligil GS.
Endoplasmic reticulum stress and the inflammatory basis of metabolic disease.
Cell. 2010 Mar 19;140(6):900-17. doi: 10.1016/j.cell.2010.02.034.

Jiao P, Ma J, Feng B, Zhang H, Diehl JA, Chin YE, Yan W, Xu H.
FFA-induced adipocyte inflammation and insulin resistance: involvement of ER stress and IKKβ pathways.
Obesity (Silver Spring). 2011 Mar;19(3):483-91.

Koji Sakai, Khristofor Agassandian, Satoshi Morimoto, Puspha Sinnayah, Martin D. Cassell, Robin L. Davisson, and Curt D. Sigmund
Local production of angiotensin II in the subfornical organ causes elevated drinking
J Clin Invest. 2007 April 2; 117(4): 1088–1095.

Mori TA
Omega-3 fatty acids and blood pressure.
Cell Mol Biol (Noisy-le-grand). 2010 Feb 25;56(1):83-92.

Ozcan L, Ergin AS, Lu A, Chung J, Sarkar S, Nie D, Myers MG Jr, Ozcan U.
Endoplasmic reticulum stress plays a central role in development of leptin resistance.
Cell Metab. 2009 Jan 7;9(1):35-51.

Purkayastha S, Zhang H, Zhang G, Ahmed Z, Wang Y, Cai D.
Neural dysregulation of peripheral insulin action and blood pressure by brain endoplasmic reticulum stress.
Proc Natl Acad Sci U S A. 2011 Feb 15;108(7):2939-44.
Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER 3rd, Simons-Morton DG, Karanja N, Lin PH; DASH-Sodium Collaborative Research Group.

Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group.
N Engl J Med. 2001 Jan 4;344(1):3-10.

Schulman IH, Zhou MS, Raij L.
Interaction between nitric oxide and angiotensin II in the endothelium: role in atherosclerosis and hypertension.
J Hypertens Suppl. 2006 Mar;24(1):S45-50.

Svetkey LP, Simons-Morton D, Vollmer WM, Appel LJ, Conlin PR, Ryan DH, Ard J, Kennedy BM.
Effects of dietary patterns on blood pressure: subgroup analysis of the Dietary Approaches to Stop Hypertension (DASH) randomized clinical trial.
Arch Intern Med. 1999 Feb 8;159(3):285-93.

Wilcox CS.
Oxidative stress and nitric oxide deficiency in the kidney: a critical link to hypertension?
Am J Physiol Regul Integr Comp Physiol. 2005 Oct;289(4):R913-35.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.