Posts

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)

References

MAIN ABSTRACT
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.

SUPPORTING ABSTRACTS
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.

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.

References

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.

References

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.

Beta-Glucans, The Healer

oatmeal-and-white-backgroundThere are quite a few products on the market that promise to heal wounds quickly. The one made from a combination of bacitracin, neomycin and polymyxin is so popular that it’s been copied as a generic. But it isn’t all-natural. For those interested in a natural alternative, there’s a new kid on the block, called beta-glucans, found in baker’s yeast and a few other common sources, and destined to be on the shelves as a gel in 2012. Heralded as a “super medicine,” beta-glucans are currently used in veterinary medicine, dietary supplements, and cosmetics. And Norwegian scientists say it has even more potential.

The Research Council of Norway announced the results of a study headed by Rolf Einar Engstad, of Biotec Pharmacon, that proclaimed, “Since the mid-1980’s we have known that these substances (beta-glucans) fight infection and have a bearing on the body’s ability to kill cancerous cells, but never knew why.”  At the start of the project, the researchers were uncertain of the efficacy of the delivery method, but in infected laboratory animals, “…determined that animals receiving beta-glucans orally acquired protection that was at least as good as rats that received an injection into their bloodstream.”  Effectiveness of topical application in the healing of wounds was welcome news.  Incisions, bed sores, diabetic ulcers, and other skin insults can be treated with topical beta-glucans.  A matter that has since been addressed is short shelf life, something that can happen to any organic material, such as organic produce.  To add to beta-glucans’ acclaim is its capacity to enhance the innate immune system, that immunity with which we are born and which is first mobilized if the body is invaded by a pathogen.  (The Research Council of Norway.  2011)

As a supplement, beta-glucans has been around for a while.  These sugars are found in the cell walls of bacteria, fungi, yeasts, algae, lichens, and plants, such as oats and barley.  Orally, they have been used for treating cholesterol, diabetes, cancer and HIV/AIDS, and for bolstering the immune systems of those suffering from chronic fatigue syndrome and emotional or physical stress.  It may be given IV post-surgery to prevent infections.  Topically, it’s been used for dermatitis, eczema, wrinkles, bedsores, radiation burns, and other skin conditions.  The enhancement of macrophage function aids in healing wounds, although the exact mechanism of this improved healing is uncertain. (Portera. 1997)  Besides that, increases in collagen manufacture have been noticed, resulting in improved tensile strength of the new wound covering.  (Browder. 1988)  The activity in this arena includes the stimulation of growth factors and the release of cytokines, regulatory proteins that mediate the immune response.  (Wei. 2002)  This results in stimulation of fibroblast (giving rise to connective tissue) collagen biosynthesis.

Yeast-based beta-glucans is being taken more and more seriously as an immune health ingredient.  Because it can stand a wide range of body pH, yeast-based product could supplant—or at least enhance—probiotics as a first line of defense against invasion by bacteria and viruses.  (Watson, 2011)

Beyond healing wounds, beta-glucans may prevent the absorption of cholesterol from the stomach and intestine when it is taken orally.  The beta-glucan found in oats led oatmeal makers to petition the FDA to allow such a claim on their labels.  The FDA agreed, as long as the amount is 10% of the product.  (Federal Register. 2002)

By injection, beta-glucans stimulate the immune system by increasing chemicals that prevent infections.  Used in immunotherapy, as in treating certain invasive diseases, beta-glucans incites cytotoxicity (cell toxicity) in neoplastic (abnormal new growth) tissue while leaving healthy tissue alone.  (Vetvicka. 1996)

As with any promising developments in alternative approaches to wellness, funding for additional studies becomes a roadblock.  The promise of beta-glucans, which, because it appears in food cannot be patented as a drug (yet), paints a rosy picture for treating cuts and scrapes, and perhaps for the prevention of contagious diseases and chronic illnesses.

References

Siw Ellen Jakobsen and Else Lie
Baker’s yeast aids healing
The Research Council of Norway. Published: 07.09.2011

Portera CA, Love EJ, Memore L, Zhang L, Müller A, Browder W, Williams DL.
Effect of macrophage stimulation on collagen biosynthesis in the healing wound.
Am Surg. 1997 Feb;63(2):125-31.

Browder W, Williams D, Lucore P, Pretus H, Jones E, McNamee R
Effect of enhanced macrophage function on early wound healing.
Surgery. 1988 Aug;104(2):224-30.

Wei D, Zhang L, Williams DL, Browder IW.
Glucan stimulates human dermal fibroblast collagen biosynthesis through a nuclear factor-1 dependent mechanism.
Wound Repair Regen. 2002 May-Jun;10(3):161-8.

Elaine Watson
Biothera on a roll as yeast beta-glucan moves into the mainstream
Nutra-Ingredients-USA.com.  12 September, 2011

Food and Drug Administration, HHS
Food labeling: health claims; soluble dietary fiber from certain foods and coronary heart disease. Interim final rule.
Fed Regist. 2002 Oct 2;67(191):61773-83.

Vetvicka V, Thornton BP, Ross GD.
Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells.
J Clin Invest. 1996 Jul 1;98(1):50-61.

Charlotte Sissener Engstad, Rolf Einar Engstad, Jan-Ole Olsen and Bjarne Osterud
The effect of soluble beta-1,3-glucan and lipopolysaccharide on cytokine production and coagulation activation in whole blood.
Int Immunopharmacol 2(11):1585-97 (2002) t

Suzuki I, Hashimoto K, Ohno N, Tanaka H, Yadomae T.
Immunomodulation by orally administered beta-glucan in mice.
Int J Immunopharmacol. 1989;11(7):761-9.

Delatte SJ, Evans J, Hebra A, Adamson W, Othersen HB, Tagge EP.
Effectiveness of beta-glucan collagen for treatment of partial-thickness burns in children.
J Pediatr Surg. 2001 Jan;36(1):113-8.

Borchers AT, Stern JS, Hackman RM, Keen CL, Gershwin ME.
Mushrooms, tumors, and immunity.
Proc Soc Exp Biol Med. 1999 Sep;221(4):281-93.

Akramiene D, Kondrotas A, Didziapetriene J, Kevelaitis E.
Effects of beta-glucans on the immune system.
Medicina (Kaunas). 2007;43(8):597-606.

Ross GD, Vetvicka V, Yan J, Xia Y, Vetvicková J.
Therapeutic intervention with complement and beta-glucan in cancer.
Immunopharmacology. 1999 May;42(1-3):61-74.

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

Low Cholesterol And Mental Health

sad-eggsIf mental health is defined as a state of emotional and psychological well-being in which an individual is able to use his or her cognitive and emotional capabilities, function in society, and meet the ordinary demands of everyday life, then we need to take care of the garage in which this vehicle is kept.  Measures of depression and anxiety assess things such as self-disparagement, pessimism, lack of drive, apprehension, inability to relax, and irritability, to name a few.  Interestingly, these evaluations have demonstrated a relationship to low lipid and lipoprotein concentrations.

In work done at the end of the last century, an inverse association between mental challenges and total cholesterol and lipids was found.  That means when one goes up, the other goes down.  Testing young adult females, Duke University Medical Center discovered that women “…with low total cholesterol concentrations (<4.14 mmol/liter) relative to those with moderate to high cholesterol levels, were more likely to have higher scores on the NEO depression subscale…and anxiety subscale…” after adjustments were made for age, body mass index, oral contraceptive use and physical activity.  (Suarez.  1999)

Before we got too involved, it pays to know that 4.14 mmol/liter is equal to a cholesterol level of 160 mg/dL, or just plain 160.  Cholesterol is a steroid substance necessary to human life.  It forms the cell membranes in all organs and tissues of the body, is essential to the production of the hormones we need for growth, development, and reproduction, and it makes the bile acids necessary for absorption of nutrients.  Very little, if any, dietary cholesterol becomes serum cholesterol.

Back in the 1990’s it was noted that cholesterol levels below 160 were tied to excess mortality from all causes, primarily from a variety of cancers, respiratory and digestive diseases, and violent deaths from suicide and trauma.  Reasons behind low cholesterol have been ascribed to genetics, resistance to dietary sources, acute infections, and alcohol use/abuse.  (Meilahn.  1995)  If suicide is tied to depression, then it may be a legitimate effect.  Depression is twice as common among women as men, with about one in four suffering at some point in her lifetime.  The greatest vulnerability appears during the childbearing years, the time when its diagnosis is often overlooked.  The turbulence of hormones flooding a woman’s system at different times and in differing amounts can surely be a potent stressor.

Scientists in Barcelona, Spain, realized the connection of cholesterol to neuropsychiatric disease in a review of related literature that preceded their interest.  They found a link to early death, suicide and aggression, and personality disorders and dementia. (Martinez-Carpio.  2009). It appears that the good intentions of reducing what was thought to be the cause of cardiac mortality opened a different can of worms.  The Japanese explored the intrigue that was sparked when total mortality was not reduced despite reduction of mortality due to coronary heart disease, and found an increase in death rates due to suicide and accidents, many of which were tied to risky behaviors in persons with low cholesterol levels.  (Kunugi.  2001)  Does low cholesterol compromise judgment?  The U. of California conducted trials in the early 90’s to determine the cause behind the rise in suicides in men older than fifty years, and found that depression was three times more prevalent in those whose cholesterol was lower than 160.  Health status, number of chronic diseases, number of medications, and exercise seemed not to have had an adverse effect on depressive signs and symptoms. This led to the suggestion that the intentional lowering of cholesterol be more deliberate.  (Morgan. 1993)

Cedars-Sinai Medical Center, in Los Angeles, reported that serotonin, a neurotransmitter that controls impulsive behaviors, is tied to cholesterol levels at the synapses.  Low membrane cholesterol decreases the number of serotonin receptors, thereby reducing suppression of aggressive and destructive behaviors.  (Engelberg. 1992)  That magic number, 160, once again made headlines in the Netherlands, where epidemiologists discovered a higher prevalence of depression in males whose cholesterol was below that level.  (Steegmans. 2000)  Low cholesterol was cited as causative to rises in criminal violence in Sweden, following the association of reduced cholesterol values to low serotonin activity. (Golomb. 2000)  Reduced levels of total cholesterol, LDL, and HDL resulted in minimized serotonin values in personality disordered cocaine users, as reported by addiction researchers in their journal. (Buydens-Branchey. 2000)  In school-aged children, those with cholesterol values lower than 145 were three times more likely to have been suspended or expelled from school.  This is an absolute consideration, and has nothing to do with socio-economic status or ethnic background, nor with nutrition status or academic achievement.  (Zhang. 2005)

Life is supposed to be a balancing act.  Lots of us overdo something.  The balance between total cholesterol and HDL can allay fears of cardiovascular disease, despite cholesterol in the 200 range.  Cholesterol levels below 170 can make us irritable…and irritating.

References

Suarez EC.
Relations of trait depression and anxiety to low lipid and lipoprotein concentrations in healthy young adult women.
Psychosom Med. 1999 May-Jun;61(3):273-9.

Elaine N. Meilahn, MD
Low Serum Cholesterol  Hazardous to Health?
Circulation. 1995;92:2365-2366

Martínez-Carpio PA, Barba J, Bedoya-Del Campillo A.
[Relation between cholesterol levels and neuropsychiatric disorders].  [Article in Spanish]
Rev Neurol. 2009 Mar 1-15;48(5):261-4.

Kunugi H.
[Low serum cholesterol and suicidal behavior].  [Article in Japanese]
Nihon Rinsho. 2001 Aug;59(8):1599-604.

Morgan RE, Palinkas LA, Barrett-Connor EL, Wingard DL.
Plasma cholesterol and depressive symptoms in older men.
Lancet. 1993 Jan 9;341(8837):75-9.

Engelberg H.
Low serum cholesterol and suicide.
Lancet. 1992 Mar 21;339(8795):727-9.

Paul H. A. Steegmans, MD, Arno W. Hoes, MD, PhD, Annette A. A. Bak, MD, PhD, Emiel van der Does, MD, PhD and Diederick E. Grobbee, MD, PhD
Higher Prevalence of Depressive Symptoms in Middle-Aged Men With Low Serum Cholesterol Levels
Psychosomatic Medicine 62:205-211 (2000)

Beatrice A Golomb, Håkan Stattin, Sarnoff Mednick
Low cholesterol and violent crime
Journal of Psychiatric Research. Volume 34, Issue 4 , Pages 301-309, July 2000

Laure Buydens-Branchey, Marc Branchey, Jeffrey Hudson, Paul Fergeson
Low HDL cholesterol, aggression and altered central serotonergic activity
Psychiatry Research. Volume 93, Issue 2 , Pages 93-102, 6 March 2000

Zhang J, Muldoon MF, McKeown RE, Cuffe SP
Association of serum cholesterol and history of school suspension among school-age children and adolescents in the United States.
Am J Epidemiol 2005; 161:691-9.

Scanlon SM, Williams DC, Schloss P.
Membrane cholesterol modulates serotonin transporter activity
Biochemistry. 2001 Sep 4;40(35):10507-13.

Laure Buydens-Branchey,a Marc Branchey,a and Joseph R. Hibbelnb
ASSOCIATIONS BETWEEN INCREASES IN PLASMA N-3 POLYUNSATURATED FATTY ACIDS FOLLOWING SUPPLEMENTATION AND DECREASES IN ANGER AND ANXIETY IN SUBSTANCE ABUSERS
Prog Neuropsychopharmacol Biol Psychiatry. 2008 February 15; 32(2): 568–575.

BRIAN HALLAHAN, MRCPsych and MALCOLM R. GARLAND, MRCPsych
Essential fatty acids and mental health
The British Journal of Psychiatry (2005) 186: 275-277

Hillbrand M, Waite BM, Miller DS, Spitz RT, Lingswiler VM
Serum cholesterol concentrations and mood states in violent psychiatric patients: an experience sampling study.
J Behav Med 2000; 23:519-29.

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

Flaxseed, Exercise and Your Heart

flax-seed-oilThe heart is a muscle, the most important one on the list. Legs that hurt from pedaling a bike all over the county or biceps that burn from curls are little more than an annoyance. A heart that hurts can mean something more. If you happen to be a cyclist, the odds are in your favor that your heart won’t hurt. If you think about cycling or other laborious exercise without actually doing it, well, that’s a different story. One of the more common bad habits we have is that we don’t pay attention to things until they make funny noises, smell like a bad catalytic converter, quit giving off light, or stop altogether. When the heart makes odd sounds or threatens to quit, “shoulda, woulda, coulda” enters the mind. Exercise undoubtedly has a profound effect on cardiac health… and the rest of the body, too, for that matter. Suppose you could boost the impact of regular exercise on cardiovascular wellness just by adding flaxseeds to your diet. This uncomplicated act offers a host of reward.

Most of us already know about flaxseed oil, a remarkable anti-inflammatory material in its own right, but with a different profile from the seeds. The oil contains the alpha-linolenic acid (ALA) component of flaxseeds without the fiber or lignan components. Therefore, the oil may demonstrate the lipid-lowering properties of the plant without the laxative or anti-cancer character. Oils high in essential fats are not good for cooking, by the way, mostly because they’ll oxidize and become degraded by the high heat. Flax oil that is extracted with heat shortchanges the consumer with a product that is virtually useless and mostly rancid. It can be added to foods after cooking, just before hitting the table. Back to the seeds…

Recent discovery using laboratory animals indicates that the constituents of flaxseeds—ALA, lignans and fiber—add a dramatic benefit to exercise when looking at cardiac markers, lipid profiles and markers of inflammation. With the first group of test animals serving as the control, the second having induced heart attack symptoms, the third having symptoms but provided with flaxseed supplementation, and the fourth like the third but with exercise included, forty lab rats were gathered for the study. Flaxseed supplementation combined with exercise produced a significant rise in HDL and an elevation of the enzyme called PON1, which is a major anti-atherosclerosis and anti-oxidant component of HDL. Simultaneously, measures of infarction—troponin and TNF-alpha—decreased, leading the scientists to infer the protective characteristic of flaxseed combined with muscular exercise against the harmful effects of ischemic heart disease (Nounou, 2012).

Canadian investigators explored the properties of flaxseed components and their influence on cardiovascular health, finding that flax lignans, especially one called secoisolariciresinol, play a significant protective role in cardiovascular disease, particularly against ischemic events (Prasad, 2009). In the last century, consideration was given to flaxseed’s influence on hypercholesterolemia and concomitant atherosclerosis, noting that flaxseeds containing 51%-55% alpha-linolenic acid (ALA—an omega-3 fatty acid) and plant lignans could reduce hypercholesterolemic atherosclerosis by as much as 46% without lowering serum lipids. But the more interesting notation was that flaxseed with a lower level of ALA—only 2%-3%–had the same effect (Prasad, 1998), leading these researchers to conclude that the lignans rather than the omega-3 fats were responsible for the result. Recall that no lignans are found in flaxseed oil unless they are replaced after extraction. Since the early 2000’s, flaxseed has earned the moniker “functional food” (Bloedon, 2004).

Ventricular fibrillation is a severely abnormal heart rhythm that can be life threatening if heartbeat is interrupted for only a few seconds. Though not entirely definitive, some evidence presents flaxseed as able to improve vascular relaxation and inhibit the incidence of ventricular fibrillation (Bassett, 2009), while working in the wings to reduce after-meal glucose absorption and to lower markers of inflammation (Bloedon, 2004). The mechanism behind flaxseed’s heroic reputation involves synergies that are under analysis, including the modulation of cardiac ion channels, attenuation of triglyceride levels, cell signaling, anti-thrombosis activity and anti-arrhythmic effect (Adkins, 2010). In rabbits, animals whose cardiovascular systems parallel humans’, ventricular fibrillation that occurred during induced ischemia was halted and reperfusion injury was attenuated (Ander, 2004).

Concern about plant lignans and hormone-related cancers may not be well-founded, as discovered in two cohort studies that examined the association (Pinder, 2002) (Keinan-Boker, 2004). Here it was intimated that no association of plant lignans to breast cancer exists in premenopausal women (Touillaud, 2006). In fact, high lignan intake may create a 15% decrease in breast cancer risk in postmenopausal women (Velentzis, 2009). Even with prostate disease there is no significant association of phytoestrogens with cancer (Strom, 1999) (Hedelin, 2006) (Travis, 2009). In fact, dietary lignans may lower risk for prostate cancer (Heald, 2007).

Since most of us have taken increased responsibility for our health, it’s likely that we participate in some kind of exercise. Walking counts, but not to the refrigerator to get a pint of Ben and Jerry’s. Adding flaxseeds to the diet isn’t that hard. You can use 3 tablespoons of flax meal to replace 1 tablespoon of fat in a recipe. You could replace one egg with 1 tblspn of flax plus 3 tblspn of water. (Don’t even think about doing this for breakfast. It just ain’t the same, bacon or not.) You could mix it into a meatloaf, stir it into soups or smoothies, throw it onto your oatmeal, or mix it with sugar and cinnamon as a substitute dessert topping. But it has to be ground to work. Whole flaxseeds will pass right through the digestive system, taking all the benefits along with it.

References

Adkins Y, Kelley DS.
Mechanisms underlying the cardioprotective effects of omega-3 polyunsaturated fatty acids.
J Nutr Biochem. 2010 Sep;21(9):781-92.

Ander BP, Weber AR, Rampersad PP, Gilchrist JS, Pierce GN, Lukas A.
Dietary flaxseed protects against ventricular fibrillation induced by ischemia-reperfusion in normal and hypercholesterolemic Rabbits.
J Nutr. 2004 Dec;134(12):3250-6.

Bassett CM, Rodriguez-Leyva D, Pierce GN.
Experimental and clinical research findings on the cardiovascular benefits of consuming flaxseed.
Appl Physiol Nutr Metab. 2009 Oct;34(5):965-74.

Bloedon LT, Szapary PO.
Flaxseed and cardiovascular risk.
Nutr Rev. 2004 Jan;62(1):18-27.

Heald CL, Ritchie MR, Bolton-Smith C, Morton MS, Alexander FE.
Phyto-oestrogens and risk of prostate cancer in Scottish men.
Br J Nutr. 2007 Aug;98(2):388-96. Epub 2007 Apr 3.

Hedelin M, Klint A, Chang ET, Bellocco R, Johansson JE, Andersson SO, Heinonen SM, Adlercreutz H, Adami HO, Grönberg H, Bälter KA.
Dietary phytoestrogen, serum enterolactone and risk of prostate cancer: the cancer prostate Sweden study (Sweden).
Cancer Causes Control. 2006 Mar;17(2):169-80.

Horn-Ross PL, Hoggatt KJ, West DW, Krone MR, Stewart SL, Anton H, Bernstei CL, Deapen D, Peel D, Pinder R, Reynolds P, Ross RK, Wright W, Ziogas A.
Recent diet and breast cancer risk: the California Teachers Study (USA).
Cancer Causes Control. 2002 Jun;13(5):407-15.

Keinan-Boker L, van Der Schouw YT, Grobbee DE, Peeters PH.
Dietary phytoestrogens and breast cancer risk.
Am J Clin Nutr. 2004 Feb;79(2):282-8.

National Council on Strength and Fitness
Flaxseed and Exercise
Date:  Oct. 29, 2012

Nounou HA, Deif MM, Shalaby MA.
Effect of flaxseed supplementation and exercise training on lipid profile, oxidative stress and inflammation in rats with myocardial ischemia.
Lipids Health Dis. 2012 Oct 5;11(1):129.

Prasad K, Mantha SV, Muir AD, Westcott ND.
Reduction of hypercholesterolemic atherosclerosis by CDC-flaxseed with very low alpha-linolenic acid.
Atherosclerosis. 1998 Feb;136(2):367-75.

Prasad K.
Flaxseed and cardiovascular health
J Cardiovasc Pharmacol. 2009 Nov;54(5):369-77.

Strom SS, Yamamura Y, Duphorne CM, Spitz MR, Babaian RJ, Pillow PC, Hursting SD.
Phytoestrogen intake and prostate cancer: a case-control study using a new database.
Nutr Cancer. 1999;33(1):20-5.

Touillaud MS, Thiébaut AC, Niravong M, Boutron-Ruault MC, Clavel-Chapelon F.
No association between dietary phytoestrogens and risk of premenopausal breast cancer in a French cohort study.
Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2574-6.

Travis RC, Spencer EA, Allen NE, Appleby PN, Roddam AW, Overvad K, Johnsen NF, Olsen A, et al
Plasma phyto-oestrogens and prostate cancer in the European Prospective Investigation into Cancer and Nutrition.
Br J Cancer. 2009 Jun 2;100(11):1817-23. Epub 2009 May 12.

Velentzis LS, Cantwell MM, Cardwell C, Keshtgar MR, Leathem AJ, Woodside JV.
Lignans and breast cancer risk in pre- and post-menopausal women: meta-analyses of observational studies.
Br J Cancer. 2009 May 5;100(9):1492-8.

Ward H, Chapelais G, Kuhnle GG, Luben R, Khaw KT, Bingham S.
Lack of prospective associations between plasma and urinary phytoestrogens and risk of prostate or colorectal cancer in the European Prospective into Cancer-Norfolk study.
Cancer Epidemiol Biomarkers Prev. 2008 Oct;17(10):2891-4.

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

Wellness In The New Year (or any year for that matter)

wellness-roadThere are some things in life we just can’t control. The weather is a good example, but other people’s behavior runs a close second. In fact, sometimes we have a hard time controlling our own behaviors. Take a look at the last éclair in the box. Isn’t it calling your name? Although we can’t direct weather patterns, we can prepare for their uncertainties. Humans do have the wherewithal to live through a hurricane unscathed, but it takes conscious effort and self-direction. We can’t rely on other people to take care of us while they’re trying to tend to their own needs. When it comes to our personal health behaviors, only we are responsible. This we can control. Making a resolution to do it is fruitless, almost inane. Doing it is noble.

Wellness is not the same thing as health. It’s possible to suffer a chronic condition and still be well. A person who lives with a limitation may be more well than a person whose faculties are fully operational. While health may be defined as being physically, mentally and spiritually sound—maybe even financially, occupationally and socially— wellness describes a desire to enhance successful existence, one’s quality of life. Yet the definition of wellness is elusive and subjective. New models of wellness emerge regularly, existing on a continuum and being peculiar to each of us.

A sage cleric once said that ideas determine consequences, a concept based on absolute truth. Simply put, if you do this, that will happen. You can deny that black is black, and even call it dark white, but that changes nothing. The decisions you make today determine the outcome down the road. Because wellness is a process, it can always be improved, even by borrowing ideas and habits from others. Take a gander at some of these wellness ideas.  A few might make sense to you.

Indoor plants purify the air, albeit some are better at it than others. One of the best ways to improve indoor air is to quit smoking, and, if you have children, you’ll save money on doctor visits, too. Clean air also will help you in your newly-designed exercise program, even though it starts at only five minutes a day. We won’t beleaguer you with admonitions. We promise. This you can begin upon arising, while still in bed. What does the dog do when he first wakes up?  He stretches. Your blood vessels have been scrunched up all night. Stretch and open ’em up. Try to do a few sit-ups while you’re at it. Believe it or not, it’ll make a difference. Yes, it’ll take time, but some things are worth the wait. After your feet hit the floor, drink a full glass of water. A drop of lemon juice won’t hurt. You’ve been dehydrated all night—no fluids for eight hours. Your cells probably resemble dried peas or a half-inflated basketball. It’ll take about 20 minutes for the water to hit home, but when it does you’ll feel refreshed and improve the viscosity of your blood to keep it flowing the way it should.

Replacing that soda with plain or acidulated water or tea will swap hazard for benefit. The sugar in soda provides empty calories that get stored as fat if you don’t burn ‘em off. Even artificial sweeteners fool the body into thinking you ate something sweet. When the body learns it’s been fooled, it makes you hungry so you can use up all the insulin that’s now floating around, looking for something to do. Weight may increase. http://www.medicinenet.com/artificial_sweeteners/page11.htm

Have you looked into supplements?  Despite some negative press by opposing industries and their minions, they work. Fish oil does provide cardiac and anti-inflammatory profit, and high quality multi-vitamins do what they declare (Fletcher, 2002) (Gaziano, 2012). Besides, the nutrients once promised by fruits and vegetables now are in short supply because of modern farming practices, careless shipping and storage, and poor kitchen habits.

The cost of sleep deprivation—both financial and salubrious—is enormous. During this suspension of will power and consciousness the body and mind put things that have been disassembled by the day’s toils back together. Some of the factors that interfere with sleep can be controlled. Though not the simplest thing to do, interfering stress can be modified or even eliminated. Getting eight hours of sleep at least three or four times a week is a boon to health (Romeijn, 2012) (Ribeiro, 2012) (Chamorro, 2011) (Donga, 2010).

Taking care of yourself is necessary before you can be expected to take care of others. Some proactive measures, albeit controversial in particular circles, ask for more than moderate energy expenditure.

Reading labels is one. Learn what toxins are added to the kids’ vaccines and do something to avoid them, like asking the doctor to take the liquid from the middle of the vial—if vaccinations are a must. What’s the rub with vaccines?  Formaldehyde, mercury and MSG as preservatives. Getting more than one shot at a time places a heavy burden on a little body, so request dosing at intervals. Learn what additives are in your toothpaste. Got canker sores?  Look for sodium lauryl sulfate on the label (Chahine, 1997). Other personal and house care items might contribute to personal woes because of unneeded synthetic additives like perfumes, foaming agents, softeners and petroleum distillates.

Among the many steps to wellness, one of the most effective is realizing that food is nourishment, not entertainment. Eat what your body needs, not what your senses of smell and taste otherwise dictate. Unburned carbs get stored as fat. Sugars—think cookies and cakes—create acids that support disease, including cancer (Liu, 2000) (Burley, 1998) (Tuyns, 1988). The wrong fats encourage vascular problems—get the essential fats instead, like omega-3 and omega-6 fatty acids. Under hydration frustrates cell activity and will cause mental fog. The more you talk about health, the more likely you are to cater to it. Who better to direct person-centered health care than the person inside?

References

Mauro Alivia, Paola Guadagni, and Paolo Roberti di Sarsina
Towards salutogenesis in the development of personalised and preventive healthcare
EPMA J. 2011 December; 2(4): 381–384.

Burley VJ.
Sugar consumption and human cancer in sites other than the digestive tract.
Eur J Cancer Prev. 1998 Aug;7(4):253-77.

Chahine L, Sempson N, Wagoner C.
The effect of sodium lauryl sulfate on recurrent aphthous ulcers: a clinical study.
Compend Contin Educ Dent. 1997 Dec;18(12):1238-40.

Chamorro RA, Durán SA, Reyes SC, Ponce R, Algarín CR, Peirano PD.
[Sleep deprivation as a risk factor for obesity].
Rev Med Chil. 2011 Jul;139(7):932-40. Epub 2011 Sep 16.

Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, Corssmit EP, Romijn JA.
A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects.
J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8. Epub 2010 Apr 6.

Fletcher RH, Fairfield KM.
Vitamins for chronic disease prevention in adults: clinical applications.
JAMA. 2002 Jun 19;287(23):3127-9.

Gaziano JM, Sesso HD, Christen WG, Bubes V, Smith JP, MacFadyen J, Schvartz M, Manson JE, Glynn RJ, Buring JE.
Multivitamins in the prevention of cancer in men: the Physicians’ Health Study II randomized controlled trial.
JAMA. 2012 Nov 14;308(18):1871-80.

Albert Lee, Andrew Kiyu, Helia Molina Milman, and Jorge Jimenez
Improving Health and Building Human Capital Through an Effective Primary Care System
J Urban Health. 2007 May; 84(Suppl 1): 75–85.

Simin Liu, Walter C Willett, Meir J Stampfer, Frank B Hu, Mary Franz, Laura Sampson, Charles H Hennekens, and JoAnn E Manson
A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women1,2,3
Am J Clin Nutr June 2000 vol. 71 no. 6 1455-1461

Ronald W. Manderscheid, PhD, Director, Carol D. Ryff, PhD, Elsie J. Freeman, MD, MPH, Lela R. McKnight-Eily, PhD, Satvinder Dhingra, MPH, and Tara W. Strine, MPH
Evolving Definitions of Mental Illness and Wellness
Prev Chronic Dis. 2010 January; 7(1): A19.

McMahon S, Fleury J.
Wellness in older adults: a concept analysis.
Nurs Forum. 2012 Jan-Mar;47(1):39-51. doi: 10.1111/j.1744-6198.2011.00254.x.

Mullen KD.
Wellness: the missing concept in health promotion programming for adults
Health Values. 1986 May-Jun;10(3):34-7.

Ribeiro S.
Sleep and plasticity.
Pflugers Arch. 2012 Jan;463(1):111-20. Epub 2011 Sep 27.

Romeijn N, Verweij IM, Koeleman A, Mooij A, Steimke R, Virkkala J, van der Werf Y, Van Someren EJ.
Cold hands, warm feet: sleep deprivation disrupts thermoregulation and its association with vigilance.
Sleep. 2012 Dec 1;35(12):1673-83. doi: 10.5665/sleep.2242.

Tuyns AJ, Kaaks R, Haelterman M.
Colorectal cancer and the consumption of foods: a case-control study in Belgium.

Nutr Cancer. 1988;11(3):189-204.

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

Gut Health, Body Health

stomachThe large intestine is seldom the topic of conversation, with the possible exception of surgeons and gastroenterologists. Most “civilians” don’t pay attention to it until it isn’t working right. The inability to move material out of it is one reason. Unusual egesta might be another. Regardless of its laid back persona, the colon is actually an interesting character. It runs from the cecum (the beginning of the large intestine, where the appendix hangs) to the rectum (the dumpster), and extends about five or six feet. If you want to be technical, the colon runs between these two points. The large intestine has no digestive function, but lubricates wastes and absorbs water and remaining salts, and stores useless stuff for eventual removal. It takes about sixteen hours to evacuate the hold. You need to know that the large intestine absorbs vitamins made by colonic bacteria, such as vitamin K and the vitamin A converted from beta-carotene.

Despite that the colon is known for removal of material, there exists inside a raft of bacteria that keep a permanent residence. In fact, there are more bacteria in the colon than cells in the body. If you have ten trillion cells in your body, you have ten times that many microbes, weighing from two to five pounds. This microflora is sometimes called the microbiome or microbiota. Whichever term is used, the activities performed by these bacteria parallel that of an organ, rivaling the metabolic capacity of the liver (MacFarlane, 2010). For example, carbohydrates are fermented to form short-chain fatty acids that support epithelial cell growth, which helps to reduce the absorption of toxic products. The flora recycle carbon and nitrogen, manufacture methane, metabolize steroids, convert lignans and phytoestrogens to other compounds and fight invasion by unwelcome species. Although people can survive without them, these bacteria are among the best of friends. Damaged or abnormal gut flora is the cause of much human agony as a prime factor in disease. Treating the microbiome with dignity and respect may prevent, or even reverse, disorders that include heart disease, autoimmune conditions, allergies and cancer (deVrese, 2008) (Garcovich, 2012).

There are hundreds of different species of micro-organisms living in the gut, more than 95% of which are anaerobic and genetically diverse. A lactobacillus is more different from a bifidobacterium than a human is from a rabbit. Identification of all species is difficult because not all can be cultured, but you can rest assured that your bacteria belong to you, remaining fairly constant throughout your life time. Talk about close friends!  The healthy bacteria provide a natural barrier against pathogenic bacteria, parasites, fungi, viruses, toxins and whatever else would wreak havoc with our health. Basically, there are half a dozen main groups:  Bacteroides, Firmicutes (Clostridia, Lactobacilli, Streptococci), Actinobacteria (Bifido-), Proteobacteria (Entero-), Fusobacteria and Verrucomicrobia. Not all of these offer salubrity. Some are so complex they almost defy taxonomy, but to our benefit, the good control the evil (Vedantam, 2003) (Beaugerie, 2004).

Analyses have determined that specific gut microbes are associated with what we eat. Some are associated with carbohydrates and some with animal proteins, fats and amino acids. It appears they come to the front of the class when it’s their turn to perform. Changing diet from one type of macro-nutrient to another can alter which bacterial strain is on stage at the time. A baby’s gut is clean and sterile until it entertains bacteria from its mother. Vaginal birth may afford bacterial strains directly from mom’s gastrointestinal tract, while caesarean might present strains from the ambient environs, including the air and the attending medical folks. The infant doesn’t establish his own microbiota for up to six months after caesarean delivery, only one month for normal birth. In any case, the microbiota shapes the development of the immune system, and the immune system in turn shapes the composition of the microbiota (Nicholson, 2012).

The influence of gut microbes on immunity is profound and, therefore, associated with long-term health, particularly since microflora is relatively stable throughout adulthood. The dynamics of the gut environment are subject to perturbations, though, such as from stresses or dietary changes. It’s comforting to know that there is considerable interest in developing modalities that can manipulate biome composition to benefit the host through a kind of metabolic communication, such as would affect obesity and type 2 diabetes (Kootte, 2012). In these matters, therapeutic pathways may be designed by enlisting short-chain fatty acids, prebiotics, bile acids and probiotics. Realizing that antibiotics are non-selective in destroying bacteria—they kill the good as well as the bad—this give us the means for resolution of myriad complaints. In general, the host immune system can prevent the overgrowth of pathogens, which, upon ingestion, fall to this complex integrated structure.

Probiotics are helpful in many cases, but are not silver bullets. When used as part of a broad nutritional protocol, they are likely effective in establishing or re-establishing a healthy microbiome. Stress management, elimination of detrimental medications and dietary interventions need to be included in such a protocol. Because they are many and varied in their composition, probiotics are often viewed tentatively until they are administered and monitored for efficacy. Eating fermented foods, like sauerkraut, yogurt and kefir, fosters a nurturing environment for your own microbiome. The florae best known are the Lactobacilli (there are more than 50 strains) and Bifidobacteria (there are more than thirty). Lacto-, in one strain or another, have been used to treat and to prevent a variety of conditions, from bacterial vaginosis to childhood abdominal distress and diarrhea, to childhood respiratory infections. Bifidobacteria comprise about 90% of the intestinal community, and appear in an infant’s gut within days of parturition, especially if breastfed. The Bifido- species has been used to address irritable bowel syndrome, dental caries, blood lipids and glucose tolerance.  A knowledgeable nutrition professional can guide you in the choice of probiotics to meet a specific need if you have one. Oh, yeah, there is a yeast probiotic, called Saccharomyces boulardii, which is quite effective in treating diarrhea associated with antibiotic use, and may even be helpful with Clostridium difficile and acne.

Hey, what about short-chain fatty acids (SCFA), especially butyrate?  We’re glad you asked. Butyrate is derived from the bacterial fermentation of resistant starches and fibers. Its multiple beneficial effects have been demonstrated beyond the colon, mostly because SCFA can be absorbed across the colonic epithelium. Now that gut health has its own fan club, what with renewed interest in the GI barrier defense system, SCFAs are the darlings of moneyed research. These 2-carbons to 5-carbons fatty acids include acetate, propionate, butyrate and valerate, but the 4-carbon butyrate is the featured performer due to its multiplicity of virtues. Among butyrate’s mechanisms of action are the regulation of gene expression, inhibition of histone deacetylase (an action which helps to make copies of DNA), sequestration of ammonia (ammonia causes cloudy thinking), mobilization of renegade fats, and clearance of biotoxins (Soret, 2010) (Fusunyan, 1999) (Yin, 2001). Because butyrate availability in the colon is lower than the other SCFAs, supplementation is highly recommended. You can’t eat enough resistant starches to make enough butyrate to be physiologically significant. However, even at low concentrations, butyrate can inhibit cell proliferation of several colon cancer lines. At high concentrations, it works like gangbusters against cancer cells while leaving healthy cells alone (Omaida, 1996) (Gamet, 1992).

The extraordinary complexity of the human microbiome is only recently revealed, despite having been known for decades. The interdependence between beneficial bacteria and the immune system demands recognition. If the florae can fight the inflammation that threatens them, they can fight whatever threatens their host.

References

Arora T, Sharma R, Frost G.
Propionate. Anti-obesity and satiety enhancing factor?
Appetite. 2011 Apr;56(2):511-5. doi: 10.1016/j.appet.2011.01.016. Epub 2011 Jan 19.

Bäckhed F, Fraser CM, Ringel Y, Sanders ME, Sartor RB, Sherman PM, Versalovic J, Young V, Finlay BB.
Defining a healthy human gut microbiome: current concepts, future directions, and clinical applications.
Cell Host Microbe. 2012 Nov 15;12(5):611-22.

Beaugerie L, Petit JC.
Microbial-gut interactions in health and disease. Antibiotic-associated diarrhoea.
Best Pract Res Clin Gastroenterol. 2004 Apr;18(2):337-52.

Bischoff SC.
‘Gut health’: a new objective in medicine?
BMC Med. 2011 Mar 14;9:24.

Calder PC, Krauss-Etschmann S, de Jong EC, Dupont C, Frick JS, Frokiaer H, Heinrich J, Garn H, et al
Early nutrition and immunity – progress and perspectives.
Br J Nutr. 2006 Oct;96(4):774-90.

Roberto Berni Canani, Margherita Di Costanzo, and Ludovica Leone
The epigenetic effects of butyrate: potential therapeutic implications for clinical practice
Clin Epigenetics. 2012; 4(1): 4.

Cummings JH, Antoine JM, Azpiroz F, Bourdet-Sicard R, Brandtzaeg P, Calder PC, Gibson GR, et al
PASSCLAIM–gut health and immunity.
Eur J Nutr. 2004 Jun;43 Suppl 2:II118-II173.

de Vrese M, Schrezenmeir J.
Probiotics, prebiotics, and synbiotics.
Adv Biochem Eng Biotechnol. 2008;111:1-66. doi: 10.1007/10_2008_097.

Fanaro S, Chierici R, Guerrini P, Vigi V.
Intestinal microflora in early infancy: composition and development
Acta Paediatr Suppl. 441: 48-55. 2003

Flint HJ, Scott KP, Louis P, Duncan SH.
The role of the gut microbiota in nutrition and health.
Nat Rev Gastroenterol Hepatol. 2012 Oct;9(10):577-89.

Fusunyan RD, Quinn JJ, Fujimoto M, MacDermott RP, Sanderson IR.
Butyrate switches the pattern of chemokine secretion by intestinal epithelial cells through histone acetylation.
Mol Med. 1999 Sep;5(9):631-40.

Gamet L, Daviaud D, Denis-Pouxviel C, Remesy C, Murat JC.
Effects of short-chain fatty acids on growth and differentiation of the human colon-cancer cell line HT29.
Int J Cancer. 1992 Sep 9;52(2):286-9.

Garcovich M, Zocco MA, Roccarina D, Ponziani FR, Gasbarrini A.
Prevention and treatment of hepatic encephalopathy: Focusing on gut microbiota.
World J Gastroenterol. 2012 Dec 14;18(46):6693-700. doi: 10.3748/wjg.v18.i46.6693.

Guarner F, Malagelada JR.
Gut flora in health and disease.
Lancet. 2003 Feb 8;361(9356):512-9.

Kootte RS, Vrieze A, Holleman F, Dallinga-Thie GM, Zoetendal EG, de Vos WM, Groen AK, et al
The therapeutic potential of manipulating gut microbiota in obesity and type 2 diabetes mellitus.
Diabetes Obes Metab. 2012 Feb;14(2):112-20.

Lin HV, Frassetto A, Kowalik EJ Jr, Nawrocki AR, Lu MM, Kosinski JR, Hubert JA, Szeto D, Yao X, Forrest G, Marsh DJ
Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms.
PLoS One. 2012;7(4):e35240. doi: 10.1371/journal.pone.0035240. Epub 2012 Apr 10.

Macfarlane S, Macfarlane GT.
Regulation of short-chain fatty acid production.
Proc Nutr Soc. 2003 Feb;62(1):67-72.

MacFarlane, George T. and McBain, Andrew J. (2010). The Human Colonic Microbiota. In Colonic Microbiota, Nutrition and Health. Glenn Gibson, Ed. Dordrecht, the Netherlands: Kluwer Academic Publishers; pp 1-25

Martin FP, Dumas ME, Wang Y, Legido-Quigley C, Yap IK, Tang H, Zirah S, Murphy GM, et al
A top-down systems biology view of microbiome-mammalian metabolic interactions in a mouse model.
Mol Syst Biol. 2007;3:112.

Martin FP, Wang Y, Sprenger N, Yap IK, Lundstedt T, Lek P, Rezzi S, Ramadan Z, van Bladeren P, et al
Probiotic modulation of symbiotic gut microbial-host metabolic interactions in a humanized microbiome mouse model.
Mol Syst Biol. 2008;4:157.

Nicholson JK, Holmes E, Kinross J, Burcelin R, Gibson G, Jia W, Pettersson S.
Host-gut microbiota metabolic interactions.
Science. 2012 Jun 8;336(6086):1262-7.

O’Hara AM, Shanahan F.
The gut flora as a forgotten organ.
EMBO Rep. 2006 Jul;7(7):688-93.

Omaida C. Velázquez MD, Howard M. Lederer MD, Dr. John L. Rombeau MD
Butyrate and the colonocyte
Digestive Diseases and Sciences. April 1996, Volume 41, Issue 4, pp 727-739

Roberfroid M, Gibson GR, Hoyles L, McCartney AL, Rastall R, Rowland I, Wolvers D, Watzl B, et al
Prebiotic effects: metabolic and health benefits.
Br J Nutr. 2010 Aug;104 Suppl 2:S1-63.

Schwiertz A, Gruhl B, Löbnitz M, Michel P, Radke M, Blaut M.
Development of the intestinal bacterial composition in hospitalized preterm infants in comparison with breast-fed, full-term infants.
Pediatr Res. 2003 Sep;54(3):393-9. Epub 2003 Jun 4.

Scott KP, Duncan SH, Louis P, Flint HJ.
Nutritional influences on the gut microbiota and the consequences for gastrointestinal health.
Biochem Soc Trans. 2011 Aug;39(4):1073-8.

Scott KP, Gratz SW, Sheridan PO, Flint HJ, Duncan SH.
The influence of diet on the gut microbiota.
Pharmacol Res. 2012 Nov 9. pii: S1043-6618(12)00207-1.

Soret R, Chevalier J, De Coppet P, Poupeau G, Derkinderen P, Segain JP, Neunlist M.
Short-chain fatty acids regulate the enteric neurons and control gastrointestinal motility in rats.
Gastroenterology. 2010 May;138(5):1772-82.

Tsai F, Coyle WJ.
The microbiome and obesity: is obesity linked to our gut flora?
Curr Gastroenterol Rep. 2009 Aug;11(4):307-13.

Vedantam G, Hecht DW.
Antibiotics and anaerobes of gut origin.
Curr Opin Microbiol. 2003 Oct;6(5):457-61.

Yin L, Laevsky G, Giardina C.
Butyrate suppression of colonocyte NF-kappa B activation and cellular proteasome activity.
J Biol Chem. 2001 Nov 30;276(48):44641-6. Epub 2001 Sep 25.

Yonezawa H, Osaki T, Hanawa T, Kurata S, Zaman C, Woo TD, Takahashi M, Matsubara S, Kawakami H, Ochiai K, Kamiya S.
Destructive effects of butyrate on the cell envelope of Helicobacter pylori.
J Med Microbiol. 2012 Apr;61(Pt 4):582-9.

*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.

References

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.

Soda And Heart Risk: And We Thought It Was Only Teeth We Had To Worry About

soda-glassDid your mother ever say, “If you know what’s good for you, you’ll…?” Know what the matter is?  Even as adults who know what’s good for us, we drop the ball as if we didn’t know what’s good for us. Some of us even put the ball down on purpose from time to time. Hey, if we don’t know what’s good for us, how are we supposed to know what’s bad for us?

Catch this newsy tidbit. A lady in Monaco (you know, the place where Grace Kelly used to hang out) made her way to the ER with a palpitating heart that played syncopated rhythms. Intermittent fainting spells were included…free. After all was said and done, it turned out that the only thing she drank for the previous sixteen years was soda—a half-gallon a day, cola at that. If you’re thinking she got her 8 x 8 (eight, 8-ounce glasses of fluids a day), she really got more than she bargained for. The water part of soda is good; the other part isn’t so good.

Ingredients in soda are basically useless. The caramel color comes from heating corn or cane sugar until it reaches the desired color. Desired? By whom? The amount of sugar in a can of regular, non-diet, soda can reach twelve teaspoons. Would you let your child eat even ten spoons of sugar right from the bowl? If a person opts for diet soda, aspartame or some other fake sweetener is in the mix. That earns a chapter of its own. Phosphoric acid adds tang and tartness, but the label doesn’t say it also erodes tooth enamel (Brown, 2007), borrows calcium from bones, and is associated with kidney problems. “Natural flavors” don’t turn soda into health food. Caffeine, we are told, is added to enhance flavor, even to non-colas. Funny thing…a panel of trained tasters couldn’t tell the difference between caffeinated and non-caffeinated colas (Keast, 2007). It adds a slight bitterness and, of course, acts as a stimulant. Soda does, however, contain less caffeine than a cup of coffee.

Caffeine is a diuretic. You well know that a cup of coffee after, say 7 PM, is gonna make you get out of bed at three in the morning. A cola nightcap might do the same thing. Excess urine production—and maybe even diarrhea—will flush potassium from the body. That’s what seems to have happened to the Monaco Miss—potassium deficit. Well, now, does that make any difference? Let’s see what potassium is all about. It’s the number one positively charged ion in the fluid inside a cell, having a sodium counterpart on the other side of the membrane. Their concentration differences create an electrochemical gradient known as membrane potential, which allows a cell to work like a battery to provide power for its function. Simply, sodium tells your fingers to pick up a pencil; potassium says to let it go. Sodium contracts, potassium relaxes. If potassium is in short supply, muscle—including the heart—keeps trying to contract without being relaxed. Not good, right? Right. It’s bad enough that most of us are potassium shy because we fail to get the 4700 milligrams a day that we need, but it’s worse that soda can dissolve what’s left. Potassium helps the heart maintain a regular beat; deficiencies cause irregularities (Poole-Wilson, 1984).

Additional concerns about caffeine intake involve weight loss “miracles” that propose to suppress appetite and increase energy. Most of us are unaware that supplements can contain caffeine without it being listed on the label. A Brazilian tea that is marketed as an energy enhancing beverage, guarana, actually has twice the caffeine of coffee. While that can zoom you up, it can also induce seizures and blurred vision (Pendleton, 2012). O.K., so caffeine keeps you awake, that is, if you’re not accustomed to it. But it is related to sleep-disordered breathing if it comes from soda, though not coffee or tea (Aurora, 2012).

Through a process called osmotic diuresis, glucose and water are eliminated in urine. The kidneys normally reabsorb water and glucose, but excess sugar interferes with normal kidney function. The extra sugar attracts water, which has to go somewhere…the drain…and it takes potassium with it (Packer, 2008) (Sharma, 2013). And then there’s the likelihood that fructose will elevate uric acid levels and cause gout (Choi, 2008). Gosh, heart trouble or arthritic agony?  Choices, choices.

If you’ve been a heavy soda drinker for years, it only takes a week to set things straight. The CDC says that fewer than two percent of us get enough potassium (Cogswell, 2012). Potassium-rich foods aren’t that hard to find. Sweet and white potatoes, beet greens, tomatoes, bananas, orange, prune and tomato juices, spinach, sunflower seeds and molasses are some of the foods to consider. Keeping soda to less than a pint a day could keep you out of the ER. There are some places you really don’t need to be.

References

Aurora RN, Crainiceanu C, Caffo B, Punjabi NM.
Sleep-disordered breathing and caffeine consumption: results of a community-based study.
Chest. 2012 Sep;142(3):631-8.

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.

Brown CJ, Smith G, Shaw L, Parry J, Smith AJ
The erosive potential of flavoured sparkling water drinks.
Int J Paediatr Dent. 2007 Mar;17(2):86-91.

Brown CM, Dulloo AG, Montani JP.
Sugary drinks in the pathogenesis of obesity and cardiovascular diseases.
Int J Obes (Lond). 2008 Dec;32 Suppl 6:S28-34.

Jee Woong J. Choi, Earl S. Ford, Xiang Gao, Hyon K. Choi
Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: The third national health and nutrition examination survey
Arthritis Care & Research. January 2008; Volume 59, Issue 1: pages 109–116,

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.

Corti R, Binggeli C, Sudano I, Spieker L, Hänseler E, Ruschitzka F, Chaplin WF, Lüscher TF, Noll G.
Coffee acutely increases sympathetic nerve activity and blood pressure independently of caffeine content: role of habitual versus nonhabitual drinking.
Circulation. 2002 Dec 3;106(23):2935-40.

Fukumoto M, Yamashiro N, Kobayashi F, Nagasaka T, Takiyama Y.
A case of hypokalemic myopathy induced by excessive drinking of a beverage containing green tea extract.
Rinsho Shinkeigaku. 2013;53(3):239-42.

Griffiths RR, Vernotica EM.
Is caffeine a flavoring agent in cola soft drinks?
Arch Fam Med. 2000 Aug;9(8):727-34.

Harvard Health Letter. Aug. 2012; 37(10): 4
Do you really need that diet soda?

He FJ, Marciniak M, Carney C, Markandu ND, Anand V, Fraser WD, Dalton RN, Kaski JC, MacGregor GA.
Effects of potassium chloride and potassium bicarbonate on endothelial function, cardiovascular risk factors, and bone turnover in mild hypertensives.
Hypertension. 2010 Mar;55(3):681-8.

Keast RS, Riddell LJ.
Caffeine as a flavor additive in soft-drinks.
Appetite. 2007 Jul;49(1):255-9. Epub 2006 Dec 26.

Lutsey PL, Steffen LM, Stevens J.
Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study.
Circulation. 2008 Feb 12;117(6):754-61.

O’Keefe JH, Bhatti SK, Patil HR, Dinicolantonio JJ, Lucan SC, Lavie CJ.
Effects of Habitual Coffee Consumption on Cardiometabolic Disease, Cardiovascular Health, and All-cause Mortality.
J Am Coll Cardiol. 2013 Jul 3. pii: S0735-1097(13)02601-6.

Packer CD.
Chronic hypokalemia due to excessive cola consumption: a case report.
Cases J. 2008 Jul 14;1(1):32.

Pendleton M, Brown S, Thomas C, Odle B.
Potential toxicity of caffeine when used as a dietary supplement for weight loss.
J Diet Suppl. 2012 Dec;9(4):293-8.

Poole-Wilson PA.
Potassium and the heart.
Clin Endocrinol Metab. 1984 Jul;13(2):249-68.

Sharma R, Guber HA.
Cola-induced hypokalemia-a case report and review of the literature.
Endocr Pract. 2013 Jan-Feb;19(1):e21-3. doi: 10.4158/EP12241.CR.

Striegel-Moore RH, Thompson D, Affenito SG, Franko DL, Obarzanek E, Barton BA, Schreiber GB, Daniels SR, Schmidt M, Crawford PB.
Correlates of beverage intake in adolescent girls: the National Heart, Lung, and Blood Institute Growth and Health Study.
J Pediatr. 2006 Feb;148(2):183-7.

Temple JL, Dewey AM, Briatico LN.
Effects of acute caffeine administration on adolescents.
Exp Clin Psychopharmacol. 2010 Dec;18(6):510-20.

Tsimihodimos V, Kakaidi V, Elisaf M.
Cola-induced hypokalaemia: pathophysiological mechanisms and clinical implications.
Int J Clin Pract. 2009 Jun;63(6):900-2.

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