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Colorful Foods—Black

fresh-black-currantIf a plant had cognitions, whereby it could think and perceive, it almost assuredly would pay attention to the environmental and predatory insults that bombard it regularly, never thinking that the chemicals it makes to protect itself could likewise benefit its animated aggressors. Plants defend themselves against oxidation, pests, and harmful ultra-violet radiation by making substances that people and animals can borrow to fend off sickness and disease, and to change the way the body reacts to the insults it might receive from bacteria, viruses, and renegade cell division.

“Black foods may be richer in antioxidants than their paler counterparts,” says the September, 2011 edition of Environmental Nutrition.  A class of flavonoids called anthocyanins colors dark foods, including black beans, black carrots, black rice, black quinoa, and a few others.  “Anthocyanins act as antioxidants and anti-inflammatory agents, fending off the development of chronic diseases, such as Alzheimer’s disease, diabetes, heart disease, and certain types of cancer,” notes the writer. (Ask EN. Sept. 2011—subscription required)

Few people associate the color black with food, forgetting about blackberries, black currants, and black tea.  Whether these and other foods are really black might be debatable, but science says these foods are rich in substances that offer a host of health benefits.  Black rice, for example, is more purplish than black, but when uncooked looks black.  It’s been highly treasured in Asia for centuries, where it’s been honored for the prevention of cancers, diabetes heart disease, and Alzheimer’s disease.  (Guo. 2007)  (Ling. 2001)  High in nutritional value, black rice has substantial iron and fiber.

The anthocyanin pigments found in all the black foods have demonstrated the capacity to delay the onset of illness by suppressing the activity of chemicals that promote chronic inflammation and disease, most notably one called nuclear factor-kappa B.  (Karlsen. 2007)  There is speculation that anthocyanins do not remain intact once inside the body since they may be treated as alien compounds, but that they do their work by initiating multiple other mechanisms, such as cell signaling, increases in uric acid, and precise gene expression, particularly in matters of cancer and heart disease. (Wrolstad. 2001)   (Stauth. 2007)

Superior protein and amino acid balance, and high levels of calcium, phosphorus, iron, most B vitamins, zinc and lysine characterize black quinoa, a grain reputed as a high-endurance food from the Andes.  It’s possible that quinoa provides more essential nutrients than any other single food.  (Ruales. 1992)  Black beans have been shown to provide nutritional support to the digestive system, especially the colon.  It appears to be the ideal mix of substances for allowing colonic bacteria to produce butyric acid, the fuel for many beneficial bacterial activities, lowering the risk for colon cancer among them.  (Hangen. 2002)  Black lentils and black soybeans are other legumes with remarkable health benefits.  Because legumes lack the amino acid methionine, it’s a good idea to combine them with a grain, which lacks lysine, to get all the essential amino acids.  Soybeans are the exception, since they have a complete amino acid profile, as does the grain, quinoa.  Black soy promotes apoptosis in prostate hyperplasia and certain gastric cancer cells, and reduces prostate weight.  (Jang. 2010) (Zou. 2011)

There are more black foods than we have the means to address here, but we can’t omit the berries.  Overwhelming evidence suggest that berries, in general, have beneficial effects against several types of human cancers.  While we know about the anthocyanins, there may be unidentified compounds that have, or initiate, activities that fight cancer.  They work by counteracting and repairing damage resulting from oxidative stress and inflammation, and are able to regulate carcinogenic and xenobiotic pathways.  Being able to sensitize tumors to chemotherapy, blackberries enhance such therapy.  (Seeram. 2008)

The shade of black upon a shiny white plate is a dramatic presentation, but what it portends for the body is even more so.  For foods that can be frozen or otherwise stored when out of season, it’ll pay to stock up when you can.

References

Dramatic Nutrition in Black Foods
Chefs know that the deep, glossy shade of say black quinoa or black rice can do wonders for the visual appeal of a meal. But are there any nutritional rewards that come along with this elegant color palette? It seems like brightly colored fruits and vegetables, such as scarlet tomatoes and verdant spinach get all of the attention in the nutrition world. But you might be surprised to find out that the color black is a calling card for a plant’s health-protective nutrient load.

Guo H, Ling W, Wang Q, Liu C, Hu Y, Xia M, Feng X, Xia X
Effect of anthocyanin-rich extract from black rice (Oryza sativa L. indica) on hyperlipidemia and insulin resistance in fructose-fed rats.
Plant Foods Hum Nutr. 2007 Mar;62(1):1-6.

Ling WH, Cheng QX, Ma J, Wang T.
Red and black rice decrease atherosclerotic plaque formation and increase antioxidant status in rabbits.
J Nutr. 2001 May;131(5):1421-6.

Karlsen A, Retterstøl L, Laake P, Paur I, Kjølsrud-Bøhn S, Sandvik L, Blomhoff R.
Anthocyanins inhibit nuclear factor-kappaB activation in monocytes and reduce plasma concentrations of pro-inflammatory mediators in healthy adults.
J Nutr. 2007 Aug;137(8):1951-4.

Ronald E. Wrolstad, Ph.D.
The Possible Health Benefits of Anthocyanin Pigments and Polyphenolics
http://lpi.oregonstate.edu/ss01/anthocyanin.html.  May 2001

David Stauth
Studies force new view on biology of flavonoids
http://www.eurekalert.org/pub_releases/2007-03/osu-sfn030507.php
Public release date: 5-Mar-2007

Ruales J, Nair B
Nutritional quality of the protein in quinoa (Chenopodium quinoa, Willd) seeds.
Plant Foods Hum Nutr. 1992 Jan;42(1):1-11.

Hangen L, Bennink MR
Consumption of black beans and navy beans (Phaseolus vulgaris) reduced azoxymethane-induced colon cancer in rats.
Nutr Cancer. 2002;44(1):60-5.

Jang H, Ha US, Kim SJ, Yoon BI, Han DS, Yuk SM, Kim SW.
Anthocyanin extracted from black soybean reduces prostate weight and promotes apoptosis in the prostatic hyperplasia-induced rat model.
J Agric Food Chem. 2010 Dec 22;58(24):12686-91.

Zou Y, Chang SK.
Effect of black soybean extract on the suppression of the proliferation of human AGS gastric cancer cells via the induction of apoptosis.
J Agric Food Chem. 2011 May 11;59(9):4597-605.

Seeram NP.
Berry fruits for cancer prevention: current status and future prospects.
J Agric Food Chem. 2008 Feb 13;56(3):630-5.

Navindra P. Seeram
Berry Fruits: Compositional Elements, Biochemical Activities, and the Impact of Their Intake on Human Health, Performance, and Disease
J. Agric. Food Chem., 2008, 56 (3), pp 627–629

Wada L, Ou B.
Antioxidant activity and phenolic content of Oregon caneberries.
J Agric Food Chem. 2002 Jun 5;50(12):3495-500.

Thomasset S, Teller N, Cai H, Marko D, Berry DP, Steward WP, Gescher AJ.
Do anthocyanins and anthocyanidins, cancer chemopreventive pigments in the diet, merit development as potential drugs?
Cancer Chemother Pharmacol. 2009 Jun;64(1):201-11.

*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.

Statins And Diabetes: Why Didn’t They Tell Me?

heart-measureCan you tell when you’ve eaten too much ice cream? Does the eructation shake your table lamps after too many sodas? Sometimes we learn what enough is by having too much. Too bad it isn’t the same with drugs. A hundred-pound lady doesn’t need as many aspirins to get rid of a headache as a two-hundred-pound guy. And for those who take a statin because the doctor said so, why does everybody start with the same doses? With Zocor, everybody starts with 40 mg. Doesn’t anybody think that maybe 5 mg could do the trick? Hey, if one quart of white semi-gloss will cover the bathroom walls adequately, why buy a gallon unless you have a use for it elsewhere? You gonna paint those walls until the gallon is empty?

Over the last few years, the cholesterol model of cardiovascular disease is steadily being replaced by the inflammation model of CVD, putting statin drugs on the back burner because cholesterol, it is realized, has never caused a heart attack. In fact, half the scary cardiac events happen to people who have what are deemed ideal cholesterol numbers (Sachdeva, 2009). Yes, it is true that statins interfere with cholesterol manufacture by the body, not only in the liver, but also in the brain, where cholesterol is vital to the machinery of thought and function. Low cholesterol can lead to serious health issues when that machinery is interrupted.  Low cholesterol levels are associated with high total mortality, even in patients with coronary heart disease (Behar, 1997) (Krumholz, 1994).

Differences between young and old, and between male and female, are recognized in the cholesterol arena, too. The impact of total cholesterol as a risk factor for heart disease decreases with age (Waverling-Rijnsburger, 1997) and for women, whose moderately elevated cholesterol may actually be beneficial (Petursson, 2012). The age cutoff for both genders is fifty (Anderson, 1987). If this information regarding age was known ten years ago, why are TV ads so adamant about getting cholesterol values below a hundred?

The personal experiences of at least one NASA astronaut have attested to the nasty effects of statins, including transient global amnesia, impaired cognition, personality changes, myopathy, neuropathy and neuromuscular degeneration. The root of all these maladies is the inhibition of Co-enzyme Q 10, a physiologically necessary substance that is blocked by Lipitor, Zocor, Crestor and the rest of the gang. Without CoQ10, mitochondria don’t work their magic at cell metabolism, where they get to burn food for energy, oxidize fatty acids, and use the electrons supplied by CoQ10 for a host of other essential activities. The pathway that makes cholesterol also makes CoQ10 in the body. Stopping one stops the other. This is so well known that statin prescriptions in Canada—for Mevachor®, Pravachol® and Lipitor®— contain a warning about CoQ 10 depletion. Merck even filed two patents for a statin-CoQ 10 combination, no. 4,933,165 and no. 4,929,437, which expired in May and June of 2007 (Koon, 2013). And you thought the drug companies had your best interest at heart, eh? The cholesterol issue is a complicated one and now, to add to the quagmire of hits and misses, is the notice that statins are implicated in the risk of developing diabetes. The endearing stars in this drama are atorvastatin (Lipitor), rosuvastatin (Crestor) and simvastatin (Zocor), brought to you by Pfizer, AstraZeneca and Merck. Atorvastatin was found to be the most influential of the three at elevating blood glucose, followed by rosuvastatin and simvastatin, in a recent Canadian study carried out at the Toronto General Hospital (Carter, 2013). From this work it may be drawn that pravastatin (Pravachol) is the safest drug related to diabetes onset. Regardless of drug of choice, or rather the physician’s choice, dose intensity also seems to make a difference in diabetes risk. Intense doses, especially at 80 mg of Zocor, increase the odds of all statin-induced adverse events (Silva, 2007), extending diabetes risk to almost ten percent of the medicated population (Preiss, 2011).

For all the hoopla that accompanied statins’ debut forty years ago into the pharmaceutical world, recounting their anti-cholesterol beneficence, it’s been discovered that their real claim to fame is being anti-inflammatory. That characteristic, it’s claimed, is more important to their raison d’etre than disrupting the cholesterol (and CoQ 10) pathway (Antonopoulos, 2012) (Mora, 2006) (Weitz-Schmidt, 2002). If so, then anti-inflammatory substances that have zero side effects might be considered. In this list will be simple things with complex mechanisms, like ginger, curcumin (from turmeric), capsaicin (from hot peppers), garlic, fish oil, bromelain (from pineapples), flaxseed oil, and zinc, among others. Aside from an allergic reaction which you already would know about, the only side effects of these ingredients are possibly foul breath (that would be the anti-vampire action) and stomach upset from too much of a good thing.

The mention of CoQ10 needs at least a little thought. Natural stores of this enzyme diminish with age. The fact that it donates electrons to multiple body processes bespeaks its importance to full function. It’s comparable to using the correct gauge extension cord with an electric weed trimmer. If the cord can’t carry the voltage, the trimmer will not work to its potential. Adding CoQ 10 to the daily regimen is a prudent decision whether taking a statin or not. Why?  It helps to control blood glucose (Kolahdouz, 2013) (Mezawa, 2012).

References

Anderson KM, Castelli WP, Levy D.
Cholesterol and mortality. 30 years of follow-up from the Framingham study.
JAMA. 1987 Apr 24;257(16):2176-80.

Antonopoulos AS, Margaritis M, Lee R, Channon K, Antoniades C.
Statins as anti-inflammatory agents in atherogenesis: molecular mechanisms and lessons from the recent clinical trials.
Curr Pharm Des. 2012;18(11):1519-30.

Behar S, Graff E, Reicher-Reiss H, Boyko V, Benderly M, Shotan A, Brunner D.
Low total cholesterol is associated with high total mortality in patients with coronary heart disease. The Bezafibrate Infarction Prevention (BIP) Study Group.
Eur Heart J. 1997 Jan;18(1):52-9.

Carter AA, Gomes T, Camacho X, Juurlink DN, Shah BR, Mamdani MM.
Risk of incident diabetes among patients treated with statins: population based study.
BMJ. 2013 May 23;346:f2610. doi: 10.1136/bmj.f2610.

Richard Deichmann, MD, Carl Lavie, MD, and Samuel Andrews, MD
Coenzyme Q10 and Statin-Induced Mitochondrial Dysfunction
Ochsner J. 2010 Spring; 10(1): 16–21.

Forette B, Tortrat D, Wolmark Y.
Cholesterol as risk factor for mortality in elderly women.
Lancet. 1989 Apr 22;1(8643):868-70.

Halfdan Petursson MD, Johann A. Sigurdsson MD Dr med, Calle Bengtsson MD Dr med,
Tom I. L. Nilsen Dr Philos and Linn Getz MD PhD
Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study
Journal of Evaluation in Clinical Practice 18 (2012) 159–168

Risto Huupponen, Jorma Viikari
Statins and the risk of developing diabetes
BMJ. 23 MAY 2013;346:f3156

Kolahdouz Mohammadi R, Hosseinzadeh-Attar MJ, Eshraghian MR, Nakhjavani M, Khorami E, Esteghamati A.
The effect of coenzyme Q10 supplementation on metabolic status of type 2 diabetic patients.
Minerva Gastroenterol Dietol. 2013 Jun;59(2):231-6.

Koon, Robin
CoQ 10 Supplementation with Statins
Natural Products Insider. Feb 26, 2013

Kozarevic D, McGee D, Vojvodic N, Gordon T, Racic Z, Zukel W, Dawber T.
Serum cholesterol and mortality: the Yugoslavia Cardiovascular Disease Study.
Am J Epidemiol. 1981 Jul;114(1):21-8.

Krumholz HM, Seeman TE, Merrill SS, Mendes de Leon CF, Vaccarino V, Silverman DI, Tsukahara R, Ostfeld AM, Berkman LF.
Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years.
JAMA. 1994 Nov 2;272(17):1335-40.

Mezawa M, Takemoto M, Onishi S, Ishibashi R, Ishikawa T, Yamaga M, Fujimoto M, Okabe E, He P, Kobayashi K, Yokote K.
The reduced form of coenzyme Q10 improves glycemic control in patients with type 2 diabetes: an open label pilot study.
Biofactors. 2012 Nov-Dec;38(6):416-21.

Mora S, Ridker PM.
Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER)–can C-reactive protein be used to target statin therapy in primary prevention?
Am J Cardiol. 2006 Jan 16;97(2A):33A-41A.

Steven E. Nissen, M.D., E. Murat Tuzcu, M.D., Paul Schoenhagen, M.D., Tim Crowe, B.S., et al
Statin Therapy, LDL Cholesterol, C-Reactive Protein, and Coronary Artery Disease
N Engl J Med. January 6, 2005; 352:29-38

Preiss D, Seshasai SR, Welsh P, Murphy SA, Ho JE, Waters DD, DeMicco DA, Barter P, et al
Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a meta-analysis.
JAMA. 2011 Jun 22;305(24):2556-64.

Paul M Ridker, M.D., Christopher P. Cannon, M.D., David Morrow, M.D., Nader Rifai, Ph.D, et al
C-Reactive Protein Levels and Outcomes after Statin Therapy
N Engl J Med. Jan 6, 2005; 352:20-28

Rudman D, Mattson DE, Nagraj HS, Caindec N, Rudman IW, Jackson DL.
Antecedents of death in the men of a Veterans Administration nursing home.
J Am Geriatr Soc. 1987 Jun;35(6):496-502.

Sachdeva A, Cannon CP, Deedwania PC, Labresh KA, Smith SC Jr, Dai D, Hernandez A, Fonarow GC.
Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines.
Am Heart J. 2009 Jan;157(1):111-117.e2.

Sattar N, Preiss D, Murray HM, Welsh P, Buckley BM, de Craen AJ, Seshasai SR et al
Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials.
Lancet. 2010 Feb 27;375(9716):735-42.

Sattar N, Taskinen MR.
Statins are diabetogenic–myth or reality?
Atheroscler Suppl. 2012 Aug;13(1):1-10.

Shah RV, Goldfine AB.
Statins and risk of new-onset diabetes mellitus.
Circulation. 2012 Oct 30;126(18):e282-4. doi: 10.1161/CIRCULATIONAHA.112.122135.

Silva M, Matthews ML, Jarvis C, Nolan NM, Belliveau P, Malloy M, Gandhi P.
Meta-analysis of drug-induced adverse events associated with intensive-dose statin therapy.
Clin Ther. 2007 Feb;29(2):253-60.

Simsek S, Schalkwijk CG, Wolffenbuttel BH.
Effects of rosuvastatin and atorvastatin on glycaemic control in Type 2 diabetes—the CORALL study.
Diabet Med. 2012 May;29(5):628-31.

Sukhija R, Prayaga S, Marashdeh M, Bursac Z, Kakar P, Bansal D, Sachdeva R, Kesan SH, Mehta JL.
Effect of statins on fasting plasma glucose in diabetic and nondiabetic patients.
J Investig Med. 2009 Mar;57(3):495-9.

Gabriele Weitz-Schmidt
Statins as anti-inflammatory agents
Trends in Pharmacological Sciences, 1 Oct 2002; Vol 23, Iss 10: 482-487,

Weverling-Rijnsburger AW, Blauw GJ, Lagaay AM, Knook DL, Meinders AE, Westendorp RG.
Total cholesterol and risk of mortality in the oldest old.
Lancet. 1997 Oct 18;350(9085):1119-23.

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

Diabetes Management: Dietary Interventions

diabetes-mangmntDiabetes, the word, is loosely derived from a Greek translation of “one that straddles,” probably referring to a person who urinates frequently. You already know this is considered a metabolic disease of several types, marked by frequent urine discharge, persistent thirst, and the inability to process sugars in the diet due to a decrease in, or absence of, insulin production. There also may be target tissue insulin resistance. Type 1 diabetes mellitus is one of the two major types. Here, the symptoms arise abruptly, often in early adolescence, and the person relies on exogenous insulin to sustain life. Onset may occur at any age, though. Among other miseries, type 1 affects blood vessel health (especially the tiny ones), and manifests in the retina, kidneys, and the underlying connective layer of arterioles. Type 2 diabetes often strikes between ages thirty and forty, with gradual onset that shows few symptoms of metabolic disturbance, at least not right away. With good fortune and careful management, there may be no need for exogenous insulin; diet and perhaps oral hypoglycemic medications can do the trick. Insulin response in type 2 is delayed or reduced, but insulin secretion is not necessarily absent. In this disorder blood vessels of various sizes are affected, particularly the large ones. This can lead to premature atherosclerosis, sometimes followed by myocardial infarction and stroke. Neither of these types of diabetes is to be taken lightly. There is also a third type of diabetes, diabetes insipidus, usually caused by hormone or kidney anomalies.

You might have heard people refer to themselves as having “a touch of diabetes.”  That’s the equivalent of being a little bit pregnant. Either you are, or you aren’t. Maybe you’ll hear folks say their sugar is “a little high.”  Either expression hints that diabetes is not a serious matter. That is wrong. Managing diabetes may not be the easiest thing in the world, but it certainly is achievable, and in the long run it’s well worth the effort. When your blood sugar is normal, you feel better—you have more energy, are less tired and thirsty, have fewer skin or bladder infections, you heal faster, and you have fewer problems with your vision, teeth and feet. Taking care of yourself will avoid heart attack and stroke, the possibility of blindness, nerve damage that causes tingling and numbness in hands and feet, kidney disease that may kill you, and gum disease that causes tooth loss. Hmm, this is serious business.

Unfortunately, the body is not modular in that an organ can be removed and replaced when the warranty is near expiration. It’s not like rotating tires. Even artificial joints don’t come with grease fittings. We have to make parts last as long as possible, despite that some can be replaced…an uncomfortable though to many of us. Prevention is still the best cure. Diabetes can lead to cardiovascular damage. Yes, eyesight and nerves can be damaged, too, but space restricts us to one topic at a time. Changes in the body don’t necessarily happen independently. The cycle of progressive vascular damage from diabetes affects the heart. Changing how we eat can manage glucose levels and prevent heart disease.  One dietary technique follows the glycemic index (GI), which is a measure of how fast blood sugar rises in response to a certain food.  The index estimates how much a gram of carbohydrate elevates blood sugar after consumption, relative to consumption of pure glucose, which is given an index value of 100. Subjects with diabetes managed only by a diet focusing on optimal glycemic control were found to have reduced postprandial glucose levels, accompanied by lower markers of inflammation, notably C-reactive protein (CRP), and improved lipid panels (Wolever, 2008). From time to time, meta-analyses are employed to examine relationships among disease-causing variables. Scrutinizing the GI relationship to CVD, Australian scientists, whose colleagues are credited with designing the GI, discovered a reduction in the risk for cardiovascular disease among diabetes patients who complied with the low GI regimen (Barclay, 2008). The low GI has such potential in the management of chronic disease that those who are morbidly obese may find heart-healthy value in following the plan (Ebbeling, 2005). Even in cases where diabetes is poorly controlled, adhering to the low GI diet has merit when combined with reduced carbohydrate intake in modulating CVD risk factors, including glycated hemoglobin, called HbA1c ( Afaghi, 2012) (Eskesen, 2013) (Zhang, 2012).  Glycated hemoglobin is formed through a non-enzyme pathway when hemoglobin is exposed to high plasma levels of glucose. Glycation forms end products that cause extreme oxidative stress on the body, affecting nearly every cell and molecule. The advanced glycation end products, termed AGE’s, increase vascular permeability, inhibit vascular dilation (and elevate blood pressure), interfere with nitric oxide production (which allows blood vessels to dilate), oxidize LDL, and excite excretion of cytokines. These pathological states invite cardiac entanglement, but can be managed successfully through dietary modification.

The Mediterranean Diet has been touted for its cardiovascular benefits, but little attention has been paid to its effect on diabetes issues.  This diet is a relative newcomer to us, although it’s been a way of life in the Mediterranean for years, generally in the less opulent areas of southern Italy, parts of Greece and a few islands. Despite being called such, this diet is not typical of the entire area. For instance, wine is avoided by the Muslims of the region, and butter, lard and other animal fats comprise part of the cuisine of various indigenous groups. One thing that is easily identifiable about this regional lifestyle is ambulation—everybody walks everywhere. You know very well that accounts for a lot. The diet is abundant in plant foods. Fruit is dessert, as opposed to the sugary stuff Americans eat. The main fat is olive oil; cheese and yogurt are the chief dairy products; red meat is more an accoutrement than a feature. Legumes, unrefined non-GMO cereals, huge amounts of fruits and vegetables, moderate consumption of fish and poultry, and little saturated fat are the norm.

A cohort of more than thirteen thousand Spanish university graduates was followed for four years to assess an association of diet and diabetes. Participants who followed the Mediterranean protocol had a lower risk of disease (Martinez-Gonzalez, 2008) (Dominguez, 2012). There was no beating about the bush in this report. The conclusion was stated with conviction. At the same time, it was noted that seduction by the typical Western diet of fast and prepared foods leads to increases in cardiovascular and metabolic complications (Tarabusi, 2010).

In all the controlled trials reviewed in recent years, those that featured low GI, low carbohydrate and Mediterranean diets all led to greater improvement in glycemic control, with the Mediterranean having the most profound influence on both glucose control and weight loss, enhanced by increases in HDL (Ajala, 2013). Reduction in markers of inflammation and decreases in AGE’s are among the goals in the management of blood glucose and coronary health. AGE’s affect the physiological profiles of proteins by creating cross-links, and they induce vascular dysfunction by stiffening blood vessels and myocardial tissue. Keeping HbA1c where your doctor wants it will keep you alive long enough to be chastised for decades.

References

Abiemo EE, Alonso A, Nettleton JA, Steffen LM, Bertoni AG, Jain A, Lutsey PL.
Relationships of the Mediterranean dietary pattern with insulin resistance and diabetes incidence in the Multi-Ethnic Study of Atherosclerosis (MESA).
Br J Nutr. 2012 Aug 30:1-8.

Afaghi A, Ziaee A, Afaghi M.
Effect of low-glycemic load diet on changes in cardiovascular risk factors in poorly controlled diabetic patients.
Indian J Endocrinol Metab. 2012 Nov;16(6):991-5.

Ajala O, English P, Pinkney J.
Systematic review and meta-analysis of different dietary approaches to the management of type 2 diabetes.
Am J Clin Nutr. 2013 Mar;97(3):505-16.

Anastasios S Dontas, Nicholas S Zerefos, Demosthenes B Panagiotakos, and Dimitrios A Valis
Mediterranean diet and prevention of coronary heart disease in the elderly
Clin Interv Aging. 2007 March; 2(1): 109–115.

Barclay AW, Petocz P, McMillan-Price J, Flood VM, Prvan T, Mitchell P, Brand-Miller JC.
Glycemic index, glycemic load, and chronic disease risk–a meta-analysis of observational studies.
Am J Clin Nutr. 2008 Mar;87(3):627-37.

Bédard A, Riverin M, Dodin S, Corneau L, Lemieux S.
Sex differences in the impact of the Mediterranean diet on cardiovascular risk profile.
Br J Nutr. 2012 Oct 28;108(8):1428-34.

Chiu CJ, Liu S, Willett WC, Wolever TM, Brand-Miller JC, Barclay AW, Taylor A.
Informing food choices and health outcomes by use of the dietary glycemic index.
Nutr Rev. 2011 Apr;69(4):231-42.

Domínguez LJ, Bes-Rastrollo M, de la Fuente-Arrillaga C, Toledo E, Beunza JJ, Barbagallo M, Martínez-González MA.
Similar prediction of decreased total mortality, diabetes incidence or cardiovascular events using relative- and absolute-component Mediterranean diet score: The SUN cohort.
Nutr Metab Cardiovasc Dis. 2012 Mar 6.

Due A, Larsen TM, Mu H, Hermansen K, Stender S, Astrup A.
Comparison of 3 ad libitum diets for weight-loss maintenance, risk of cardiovascular disease, and diabetes: a 6-mo randomized, controlled trial.
Am J Clin Nutr. 2008 Nov;88(5):1232-41.

Ebbeling CB, Leidig MM, Sinclair KB, Seger-Shippee LG, Feldman HA, Ludwig DS.
Effects of an ad libitum low-glycemic load diet on cardiovascular disease risk factors in obese young adults.
Am J Clin Nutr. 2005 May;81(5):976-82.

K. Eskesen, M. T. Jensen, S. Galatius, H. Vestergaard, P. Hildebrandt, J. L. Marott,
J. S. Jensen
Glycated haemoglobin and the risk of cardiovascular disease, diabetes and all-cause mortality in the Copenhagen City Heart Study
Journal of Internal Medicine. Vol 273, Iss 1, pp 94–101, January 2013

Hartog JW, Voors AA, Bakker SJ, Smit AJ, van Veldhuisen DJ.
Advanced glycation end-products (AGEs) and heart failure: pathophysiology and clinical implications.
Eur J Heart Fail. 2007 Dec;9(12):1146-55.

Konstantinidou V, Covas MI, Sola R, Fitó M.
Up-to date knowledge on the in vivo transcriptomic effect of the Mediterranean diet in humans.
Mol Nutr Food Res. 2013 Feb 18. doi: 10.1002/mnfr.201200613. [Epub ahead of print]

Kuhlmann M., Levin N.
Interaction between Nutrition and Inflammation in Hemodialysis Patients. in “Cardiovascular Disorders in Hemodialysis”
Ronco C. Vicenza and Brendolan A. Vicenza, editors. Basel, Karger, 2005, vol 149, pp 200-207

Lagiou P, Sandin S, Weiderpass E, Lagiou A, Mucci L, Trichopoulos D, Adami HO.
Low carbohydrate-high protein diet and mortality in a cohort of Swedish women.
J Intern Med. 2007 Apr;261(4):366-74.

Lagiou P, Sandin S, Lof M, Trichopoulos D, Adami HO, Weiderpass E.
Low carbohydrate-high protein diet and incidence of cardiovascular diseases in Swedish women: prospective cohort study.
BMJ. 2012 Jun 26;344:e4026. doi: 10.1136/bmj.e4026.

Lajous M, Boutron-Ruault MC, Fabre A, Clavel-Chapelon F, Romieu I.
Carbohydrate intake, glycemic index, glycemic load, and risk of postmenopausal breast cancer in a prospective study of French women.
Am J Clin Nutr. 2008 May;87(5):1384-91.

Talya Lavi, RD, Avraham Karasik, MD, Nira Koren-Morag, PHD, Hannah Kanety, PHD,
Micha S. Feinberg, MD, Michael Shechter, MD, MA
The Acute Effect of Various Glycemic Index Dietary Carbohydrates on Endothelial Function in Nondiabetic Overweight and Obese Subjects
College of Cardiology Vol. 53, No. 24, 2009: 2283-2287

Martínez-González MA, de la Fuente-Arrillaga C, Nunez-Cordoba JM, Basterra-Gortari FJ, Beunza JJ, Vazquez Z, Benito S, Tortosa A, Bes-Rastrollo M.
Adherence to Mediterranean diet and risk of developing diabetes: prospective cohort study.
BMJ. 2008 Jun 14;336(7657):1348-51

Martínez-González MA, García-López M, Bes-Rastrollo M, Toledo E, Martínez-Lapiscina EH, Delgado-Rodriguez M, Vazquez Z, Benito S, Beunza JJ.
Mediterranean diet and the incidence of cardiovascular disease: a Spanish cohort.
Nutr Metab Cardiovasc Dis. 2011 Apr;21(4):237-44.

Massaro M, Carluccio MA, De Caterina R.
Direct vascular antiatherogenic effects of oleic acid: a clue to the cardioprotective effects of the Mediterranean diet.
Cardiologia. 1999 Jun;44(6):507-13.

Peppa M, Raptis SA.
Advanced glycation end products and cardiovascular disease
Curr Diabetes Rev. 2008 May;4(2):92-100.

Rose Marie Robertson, MD; Lynn Smaha, MD, PhD
Can a Mediterranean-Style Diet Reduce Heart Disease?
Circulation. 2001; 103: 1821-1822

Valeria Tarabusi, Carla Cavazza, Francesca Pasqui, Alessandra Gambineri, Renato Pasquali
Quality of diet, screened by the Mediterranean diet quality index and the evaluation of the content of advanced glycation endproducts, in a population of high school students from Emilia Romagna
Mediterranean J Nutrition and Metabolism. Sep 2010, Vol 3, Iss 2, pp 153-157

Temelkova-Kurktschiev TS, Koehler C, Henkel E, Leonhardt W, Fuecker K, Hanefeld M.
Postchallenge plasma glucose and glycemic spikes are more strongly associated with atherosclerosis than fasting glucose or HbA1c level.
Diabetes Care. 2000 Dec;23(12):1830-4.

Uchiki T, Weikel KA, Jiao W, Shang F, Caceres A, Pawlak D, Handa JT, Brownlee M, Nagaraj R, Taylor A.
Glycation-altered proteolysis as a pathobiologic mechanism that links dietary glycemic index, aging, and age-related disease (in nondiabetics).
Aging Cell. 2012 Feb;11(1):1-13.

Wolever TM, Gibbs AL, Mehling C, Chiasson JL, Connelly PW, Josse RG, Leiter LA, Maheux P, Rabasa-Lhoret R, Rodger NW, Ryan EA.
The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein.
Am J Clin Nutr. 2008 Jan;87(1):114-25.

Yurong Zhang, Gang Hu, Zuyi Yuan, Liwei Chen
Glycosylated Hemoglobin in Relationship to Cardiovascular Outcomes and Death in Patients with Type 2 Diabetes: A Systematic Review and Meta-Analysis
PLoS ONE 7(8): e42551

Ziaee A, Afaghi A, Sarreshtehdari M.
Effect of low glycemic load diet on glycated hemoglobin (HbA1c) in poorly-controlled diabetes patients.
Glob J Health Sci. 2011 Dec 29;4(1):211-6.

*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.

Blood Pressure and…

bloodpressure-cuffThere is no naturally normal value for blood pressure (BP), but if yours is higher than that level deemed risky, you need to do something about it or face the possibility of some nasty consequences, such as stroke or cardiac episode, both of which can kill you—and are preventable. During each beat of the heart, pressure varies between a maximum, called systolic, and a minimum, called diastolic. The systolic pressure is the force that pushes blood out of the left ventricle; diastolic pressure refers to the heart at rest. The word diastole means dilation.

High blood pressure can cause arteries to become harder and thicker. Sometimes that can cause a bulge, an aneurysm, a weak spot in the artery that is subject to rupture, resulting in hemorrhage and probably death. Aneurysms don’t disappear by themselves, so some kind of invasive procedure might follow, depending on size and location. Copper deficiency is associated with aneurysm risk, so you might want to look at your diet, particularly if it’s high in zinc, the element some believe will improve male health and performance. But assuring copper sufficiency won’t necessarily prevent an aneurysm caused by elevated BP.

If the heart has to work harder to pump blood against the elevated pressures in the vessels, the heart muscle can get thicker, which makes it even more difficult to pump blood. This is the onset of heart failure, which may or may not be easily treated. In fortunate instances, a thickened heart can revert to normal size. Effects of continued high BP may involve the kidneys, brain and eyes. In polls, most people would rather die than face blindness (Giridhar, 2002) (Pfizer, 2008), which can result from hypertensive retinopathy.

There is no known cause of essential hypertension, but risks have been identified to include salt intake, obesity, race, physical activity, stress, heredity and diet. Secondary hypertension may be related to kidney, endocrine or neurological dysfunction. Medications, such as amphetamines and decongestants, can elevate blood pressure, as can alcohol. What is termed “normal” BP is a systolic pressure less than 120 mmHg and a diastolic pressure less than 80 mmHg (120/80). It takes a visit with your physician to determine your personal baseline and to work out a protocol if one is deemed necessary. That might include a medication besides a dietary intervention to address overweight.

Because cardiovascular disease is a leading cause of mortality in the economically developed world, much attention has been given to it. Diet and lifestyle are significant influences on cardiac risk, and may instigate abnormal lipid profiles, insulin resistance, diabetes and other pathologies suggestive of their impact. Of interest in the management of CVD risk factors are omega-3 fatty acids. Both omega-3 and omega-6 fats are considered essential; the body is unable to synthesize them. The conversion of the mother omega-3 and omega-6 fats, alpha-linolenic acid and linoleic acid, to longer-chain fatty acids, EPA/DHA and arachidonic acid, is terribly inefficient. Because omega-6 fats are held to be a dietary excess by virtue of a regimen high in processed foods and cheap supermarket oils, omega-3 fats, as fish oil, have received considerable interest. Fish oil is rich in EPA and DHA, the former having cardiovascular attributes and the latter having cerebral and retinal activity. Together, these fatty acids have induced moderate reductions in blood pressure at doses approximating 3 grams a day in both treated and untreated persons with elevated BP (Abeywardena, 2011). The mechanism explaining the activity is uncertain, but appears related to improvement in vascular endothelial function, one of these being reduction in stiffness. To address concerns about fish oil’s effect on LDL cholesterol, it is noted that the change in LDL particle size from small to large is a benefit (Ibid.).

One characteristic of hypertension is thickening of the arterial wall. In an animal model of hypertension, arterial thickening was attenuated with DHA treatment and the blood pressure decrease was compared to that induced by a beta blocker. Though only conjectural, other mechanisms by which fish oil lowers BP may involve activation of potassium channels (Toshinori, 2013). It is also possible that the anti-inflammatory compounds encouraged by fish oils ameliorate BP through a hormone-like effect that works in conjunction with the fatty acids’ blood-thinning character. Doses here approach 3 grams a day (Cabo, 2012).

In a twelve-week comparison/contrast trial pitting the omega-6 safflower oil against fish oil, the latter was found to offer significant benefit in reducing blood pressure in subjects with mild hypertension (Radack, 1991), while introducing no adverse changes in plasma lipid values. Including this with sixty-nine other random trials, researchers agree that available evidence indicates that inclusion of EPA/DHA in one’s diet reduces both systolic and diastolic BP at doses of at least 2 grams a day (Miller, 2014). Joining a fish oil protocol with a weight loss program, where applicable, wrought a 13 point drop in systolic and a 9 point drop in diastolic numbers in a cohort having a body mass index in excess of 31.0, the point at which obesity is defined (Bao, 1998).

If you take a prescription medication to keep your blood pressure controlled, don’t just stop it in favor of the fatty acids in fish oil. Doing so risks damage from BP rebound, which can cause serious damage to an artery. If you experience unwelcome side effects from your meds, talk with the doctor and look for an alternative drug. There certainly are enough of them on the market. Integrating fish oil with a BP drug is not generally a hazard, and may even be a boon. On the other hand, if BP falls too low, you can get dizzy, especially after standing from a sitting position. Essential fatty acids exist in the realm of complementary medicine, which is meant to complement, not necessarily to replace, conventional modalities in treating a variety of physical maladies. Hypertension is one that is relatively easy to manage.

References

Abeywardena MY, Patten GS.
Role of ω3 long-chain polyunsaturated fatty acids in reducing cardio-metabolic risk factors.
Endocr Metab Immune Disord Drug Targets. 2011 Sep 1;11(3):232-46.

Bao DQ, Mori TA, Burke V, Puddey IB, Beilin LJ.
Effects of dietary fish and weight reduction on ambulatory blood pressure in overweight hypertensives.
Hypertension. 1998 Oct;32(4):710-7.

Biermann J, Herrmann W.
Modification of selected lipoproteins and blood pressure by different dosages of n-3-fatty acids.
Z Gesamte Inn Med. 1990 Sep 15;45(18):540-4.

Borghi C, Cicero AF.
Omega-3 polyunsaturated fatty acids: Their potential role in blood pressure prevention and management.
Heart Int. 2006;2(2):98.

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

Cicero AF, Ertek S, Borghi C.
Omega-3 polyunsaturated fatty acids: their potential role in blood pressure prevention and management.
Curr Vasc Pharmacol. 2009 Jul;7(3):330-7.

Margolin G, Huster G, Glueck CJ, Speirs J, Vandegrift J, Illig E, Wu J, Streicher P, Tracy T.
Blood pressure lowering in elderly subjects: a double-blind crossover study of omega-3 and omega-6 fatty acids.
Am J Clin Nutr. 1991 Feb;53(2):562-72.

Miller PE, Van Elswyk M2, Alexander DD3.
Long-chain omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and blood pressure: a meta-analysis of randomized controlled trials.
Am J Hypertens. 2014 Jul;27(7):885-96.

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

Morris MC, Taylor JO, Stampfer MJ, Rosner B, Sacks FM.
The effect of fish oil on blood pressure in mild hypertensive subjects: a randomized crossover trial.
Am J Clin Nutr. 1993 Jan;57(1):59-64.

Radack K, Deck C, Huster G.
Arch Intern Med. 1991 Jun;151(6):1173-80.
The effects of low doses of n-3 fatty acid supplementation on blood pressure in hypertensive subjects. A randomized controlled trial.

Toshinori Hoshia, Bianka Wissuwab, Yutao Tiana, Nobuyoshi Tajimaa, Rong Xua, Michael Bauerb, Stefan H. Heinemannc, and Shangwei Houd
Omega-3 fatty acids lower blood pressure by directly activating large-conductance Ca2+-dependent K+ channels
PNAS March 4, 2013. Published online before print March 4, 2013

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

You Gotta Have Heart

healthy-heart-smIf you attended high school most days, you might have learned that atoms are made of protons, electrons and neutrons, having charges that are positive, negative or neutral, in that order. If the charges get out of balance, the atom is either negatively or positively charged. The switch between one type of charge and the other allows electrons to move from one atom to the next. It’s this flow of electrons that we call electricity and is the energy that controls everything about the body. This is the source of the signals that allow us to grab the doorknob or turn the ignition switch, or even to think about what to have for dinner. Instead of flowing along a continuous wire, as happens in the house, these signals jump from one cell to the next—and they do it fast.

The potassium inside a cell and the sodium outside have a lot to do with our electrical capacity. At rest, a cell has more negatively charged potassium inside than positively charged sodium. As the negatives and positives are attracted to each other, they cross the barrier between them—the cell membrane—through a gate, and create electricity in order to initiate a movement, thought or biological function. This impulse triggers the gate on the neighboring cell, then on the next one, the next one. This is how the sinoatrial (SA) node of the heart (its pacemaker) tells it to contract and how your eye tells your brain what you just saw. One of the interesting, though admittedly still painful, facets of life happens when you hit a finger with a hammer. The pain message travels through a sensory nerve to the brain in a fraction of a second, and then the brain associates the assault with discomfort before it tells you to move your finger away from the site of injury. Even though you realize what just happened, it takes a brief moment before the throbbing starts. All this is based on electrical activity. This might happen at 250 miles an hour, much slower than the 180,000 miles per second speed of electricity along a wire.

Our cells—more than 60 trillion—work hard every day to multiply themselves, digest nutrients, remove wastes and make energy from something called ATP. Inside each cell are little power plants called mitochondria, the number depending on the job of the cell. An eyelid will not have as many mitochondria as a bicep. ATP is made inside a mitochondrion, where Co-Enzyme Q 10 directs the function of the electron transport chain by collecting and transferring electrons along the chain. In its reduced form, where it gains an electron, CoQ10 acts as an antioxidant, effectively recycling vitamin E and possibly having an anti-atherogenic effect (Turunen, 2002).

Although often ignored by conventional medicine, it is important to note that CoQ10 shares a metabolic pathway with cholesterol and that stores diminish with age, whether by decreased synthesis or by increased requirements, or even by the elevated lipid peroxidation that accompanies aging. If we regulate cholesterol with a statin drug, we also regulate the manufacture of CoQ10; hence the need for supplementation to maintain the electrical grid. In the first double-blinded study ever that examined CoQ10 in cardiac interventions, it was discovered that enzyme supplementation in heart failure patients reduced hospital admissions and death by improving cardiac function through enhancement of the respiratory chain at doses of 100 mg three times a day (Mortensen, 2013).

Allopathic medicine rarely looks into the micronutrient deficiencies that either foretell or cause impaired function of the heart’s electrical circuits. Its therapeutic options are confined to treating symptoms. Cellular—or membrane—medicine recognizes the important components of the energy formation cycle. Patients who suffered congestive heart myopathies had shown remarkable responses to CoQ10 therapy when assiduously administered in a faithful regimen (Langsjoen, 1985). If such was the case decades ago, why has there been so little publicity?  New York Heart Association (NYHA) class IV heart failure defines almost complete cardiac insufficiency. Patients who were expected to die within two years under conventional therapy did not because it was recognized that CoQ10 is indispensable in mitochondrial bioenergetics (Langsjoen, 1988).

Absorption of supplemental CoQ10 on an empty stomach is poor, with more than sixty percent excreted in feces. It improves when taken with foods having a considerable lipid profile. In the presence of bile detergents lipids are broken into very small particles, thus increasing their surface area and subsequent susceptibility to the lipase enzymes that digest fats. Now, especially in the company of phosphatidylcholine, these particles are absorbed by intestinal mucosa and passed into the bloodstream. It takes about three weeks of faithful supplementation to attain maximum serum concentrations.

As with most integrative modalities, ongoing studies are welcome, but suffer lack of funding because they interfere with the profits garnered by pharmaceuticals. The number of eligible heart transplant patients surpasses the available number of donors. On the bright side, CoQ10 has a beneficial effect on these persons by virtue of providing a pharmacological bridge that offers an improvement in functional status and quality of life (Berman, 2004), including ejection fraction (Fotino, 2013).

For a long time, medicine has sought a means to return flexibility to the cardiovascular system that has succumbed to the ravages of time and insult, such as smoking, excessive sugar intake, and diets that promote advanced glycation endproducts. Patients suffering NYHA class III CHF who received supplemental CoQ10 at 100 mg tid, experienced improvement in left ventricular contractility and ejection fraction after only four weeks (Belardinelli, 2005), indicating the plausibility of such a protocol.

Studies may be clouded by anticipated outcomes, the bias of which may be directedby expectations of funding bodies. In too may instances, Eurasian investigatorsfind more successes than North Americans. The bottom line appears that low CoQ10concentrations are predictive of adverse CHF events, leaving one to understandthe rationale for intervention with the supplement. Endogenous manufacture ofCoQ10 requires sufficient vitamin B6 for biosynthesis. Most of us consume lessthan 10 mg of CoQ10 a day from dietary sources, leaving plenty of room for supplementation,even if we lack a pathology. The last thing we need is a power failure.

References

Abe, K., Matsuo, Y., Kadekawa, J., Inoue, S., and Yanagihara, T.
Effect of coenzyme Q10 in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS): evaluation by noninvasive tissue oximetry.
J Neurol.Sci. 1-1-1999;162(1):65-68.

Baggio, E., Gandini, R., Plancher, A. C., Passeri, M., and Carmosino, G.
Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure (interim analysis). The CoQ10 Drug Surveillance Investigators.
Clin Investig. 1993;71(8 Suppl):S145-S149.

Bargossi, A. M., Grossi, G., Fiorella, P. L., Gaddi, A., Di Giulio, R., and Battino, M.
Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMG-CoA reductase inhibitors.
Mol.Aspects Med 1994;15 Suppl:s187-s193.

Belaia, O. L., Kalmykova, V. I., Ivanova, L. A., and Kochergina, L. G.
[Experience in coenzyme Q10 application in complex therapy of coronary heart disease with dyslipidemia].
Klin Med (Mosk) 2006;84(5):59-62.

Belardinelli R, Muçaj A, Lacalaprice F, Solenghi M, Principi F, Tiano L, Littarru GP.
Coenzyme Q10 improves contractility of dysfunctional myocardium in chronic heart failure.
Biofactors. 2005;25(1-4):137-45.

Belardinelli R, Muçaj A, Lacalaprice F, Solenghi M, Seddaiu G, Principi F, Tiano L, Littarru GP.
Coenzyme Q10 and exercise training in chronic heart failure.
Eur Heart J. 2006 Nov;27(22):2675-81.

Berman M, Erman A, Ben-Gal T, Dvir D, Georghiou GP, Stamler A, Vered Y, Vidne BA, Aravot D.
Coenzyme Q10 in patients with end-stage heart failure awaiting cardiac transplantation: a randomized, placebo-controlled study.
Clin Cardiol. 2004 May;27(5):295-9.

Chen, R. S., Huang, C. C., and Chu, N. S.
Coenzyme Q10 treatment in mitochondrial encephalomyopathies. Short-term double-blind, crossover study.
Eur.Neurol. 1997;37(4):212-218.

Choe, J. Y., Combs, A. B., and Folkers, K.
Prevention by coenzyme Q10 of the electrocardiographic changes induced by adriamycin in rats.
Res Commun Chem Pathol Pharmacol 1979;23(1):199-202.

Crane FL.
Biochemical functions of coenzyme Q10.
J Am Coll Nutr. 2001 Dec;20(6):591-8.

Folkers K, Vadhanavikit S, Mortensen SA.
Biochemical rationale and myocardial tissue data on the effective therapy of cardiomyopathy with coenzyme Q10.
Proc Natl Acad Sci U S A. 1985 Feb;82(3):901-4.

Folkers, K., Morita, M., and McRee, J., Jr.
The activities of coenzyme Q10 and vitamin B6 for immune responses.
Biochem Biophys.Res Commun. 5-28-1993;193(1):88-92.

Folkers, K.
Heart failure is a dominant deficiency of coenzyme Q10 and challenges for future clinical research on CoQ10.
Clin Investig 1993;71(8 Suppl):S51-S54

Fotino AD, Thompson-Paul AM, Bazzano LA.
Effect of coenzyme Q₁₀ supplementation on heart failure: a meta-analysis.
Am J Clin Nutr. 2013 Feb;97(2):268-75.

Gottlieb, S. S., Khatta, M., and Fisher, M. L.
Coenzyme Q10 and Congestive Heart Failure.
Ann.Intern.Med 11-7-2000;133(9):745-746.

Hofman-Bang, C., Rehnqvist, N., Swedberg, K., Wiklund, I., and Astrom, H.
Coenzyme Q10 as an adjunctive in the treatment of chronic congestive heart failure. The Q10 Study Group.
J Card Fail. 1995;1(2):101-107.

Keogh A, Fenton S, Leslie C, Aboyoun C, Macdonald P, Zhao YC, Bailey M, Rosenfeldt F.
Randomised double-blind, placebo-controlled trial of coenzyme Q, therapy in class II and III systolic heart failure.
Heart Lung Circ. 2003;12(3):135-41.

Laaksonen, R., Ojala, J. P., Tikkanen, M. J., and Himberg, J. J.
Serum ubiquinone concentrations after short- and long-term treatment with HMG-CoA reductase inhibitors.
Eur.J Clin Pharmacol. 1994;46(4):313-317.

Langsjoen PH, Vadhanavikit S, Folkers K.
Response of patients in classes III and IV of cardiomyopathy to therapy in a blind and crossover trial with coenzyme Q10.
Proc Natl Acad Sci U S A. 1985 Jun;82(12):4240-4.

Langsjoen PH, Folkers K, Lyson K, Muratsu K, Lyson T, Langsjoen P.
Effective and safe therapy with coenzyme Q10 for cardiomyopathy.
Klin Wochenschr. 1988 Jul 1;66(13):583-90.

Langsjoen PH, Langsjoen AM.
Supplemental ubiquinol in patients with advanced congestive heart failure.
Biofactors. 2008;32(1-4):119-28.

Molyneux SL, Florkowski CM, George PM, Pilbrow AP, Frampton CM, Lever M, Richards AM.
Coenzyme Q10: an independent predictor of mortality in chronic heart failure.
J Am Coll Cardiol. 2008 Oct 28;52(18):1435-41

Mortensen SA.
Overview on coenzyme Q10 as adjunctive therapy in chronic heart failure. Rationale, design and end-points of “Q-symbio”–a multinational trial.
Biofactors. 2003;18(1-4):79-89.

SA Mortensen, A Kumar, P Dolliner, KJ Filipiak, D Pella, U Alehagen, G Steurer, GP Littarru, F Rosenfeldt
The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure. Results from the Q-SYMBIO study
European Journal of Heart Failure ( 2013 ) 15 ( S1 ), S20

Sander S, Coleman CI, Patel AA, Kluger J, White CM.
The impact of coenzyme Q10 on systolic function in patients with chronic heart failure.
J Card Fail. 2006 Aug;12(6):464-72.

Sinatra ST.
Refractory congestive heart failure successfully managed with high dose coenzyme Q10 administration.
Mol Aspects Med. 1997;18 Suppl:S299-305.

Turunen M, Wehlin L, Sjöberg M, Lundahl J, Dallner G, Brismar K, Sindelar PJ.
beta2-Integrin and lipid modifications indicate a non-antioxidant mechanism for the anti-atherogenic effect of dietary coenzyme Q10.
Biochem Biophys Res Commun. 2002 Aug 16;296(2):255-60.

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