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Sarcopenia

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Sarcopenia 

Nutritional intervention for a quiet epidemic

Sarcopenia is a complex, age related process that occurs in every aging adult patient and is virtually untreatable by pharmaceutical interventions. This article will explain the lack of available treatment and provide evidence for the use of supplemented protein to prevent and reverse muscle loss in elderly patients.

Sarcopenia research has been poor to date due to inconsistencies in diagnostic criteria and the difficulty in isolating the condition from other atrophic diseases such as cachexia and disuse atrophy. Measuring muscle with imaging has proven to be an inaccurate surrogate for muscle strength and power, the factors that account for the morbidity and mortality associated with sarcopenia (Brass 2011). Given these limitations to the research, and the known complexity of the disease, the development of therapeutic interventions has been challenging.

Early theories on the mechanisms behind age related muscle atrophy focused on increased muscle catabolism as a principle cause, however more recent evidence has shown that muscle breakdown in the elderly appears to occur at similar rates to younger cohorts (Koopman 2011). Evidence has shown that the most marked changes in the aging skeletal muscle lays in the anabolic processes responsible for increasing muscle mass in response to nutrition and exercise. The term anabolic resistance was coined to describe these processes, which include: decreasing insulin sensitivity, decreased protein synthesis in response to dietary essential amino acids (EAA) and decreased protein synthesis response to exercise.

Sarcopenia differs in both mechanism and clinical presentation from cachexia. Unlike cachexia, sarcopenia has a relative preservation of fat mass, which may cause weight loss to be masked in many patients. Evidence has shown that weight stable elderly patients should still be considered for treatment of sarcopenia (Gallagher 2000).

Drug trials have focused on increasing anabolic hormones that decline with age (testosterone and other androgens), and improving blood flow to atrophic muscles. Testosterone supplementation to hypogonadal men has shown some benefit, however given the increased risk of cardiovascular events (Basaria 2010), focus has shifted to Selective Androgen Receptor Modulators (SARMs) (Rolland 2011). Growth hormone, ghrenlin, estrogen and myostatin inhibitors have all been investigated for the treatment of sarcopenia without substantial gains in muscle mass (Rolland 2011). ACE inhibitors show promise for the treatment of muscle loss after studies found that patients treated for hypertension with ACEI were found to have a stabilization of muscle atrophy. This benefit is suspected to be due to improved blood flow to peripheral tissues (Brass 2011).

Nutritional supplementation for elderly patients must improve overall under-nutrition with a particular focus on protein intake.

Improving caloric intake alone has been shown to offer no benefit to muscle mass or function in the elderly (Milne 2009). Outlined below is the current evidence for using protein supplements for the prevention of sarcopenia as well as for treatment of reduced muscle mass. When considering protein supplementation in elderly patients factors to account for include: dose, %EAA, protein source, and timing of protein intake relative to other foods.

Current recommendations for protein intake in the elderly (0.8g/ kg/d) offer little benefit to sarcopenic patients (Morley 2010). Reviews have shown that many elderly patients do not consume the recommended 0.8g/kg/d (Kerstetter 2003, Rousset 2003) and patients who do consume this dosage are only modestly protected against muscle loss (Genaro 2010, Morley 2010). The Healthy Aging and Body Composition study demonstrated that elderly patients in the highest quartile (protein intake 1.1g/kg/d) lost 40% less appendicular lean mass than patients in the lowest quartile (0.7g/kg/d) (Houston 2008). In a recent review, Morley and colleagues discussed the evidence for increasing the recommended daily dosage of protein for aging adults to 1.0-1.6g/kg/d based on data that shows that 1.0g/kg/d is the minimum dosage required to prevent muscle loss with dosages ranging up to 1.6g/kg/d showing improvements in muscle mass (Morley 2010).

Conflicting studies exist for the timing of protein intake throughout the day as well as the positive or negative impact of combining protein intake with carbohydrates. Arnal et al (Arnal 1999) found that elderly women who consumed the majority of their protein intake at the midday meal had 80% greater protein retention than the control group as calculated by a more positive nitrogen balance. However, in a randomized controlled trial in 2009, Symons et al found that a bolous of 90 grams of animal protein (lean beef) was no more beneficial than a 30 gram bolous through direct examination of protein synthesis through vastus lateralus biopsy (Symons 2009). This more recent study suggests that an upper limit per meal is reached in patients around 30 grams. This study also provides more conclusive evidence given the direct observation of protein synthesis (through uptake of radiolabeled phenylalanine in muscle biopsy) versus calculated protein use based on nitrogen balance. Research has also suggested supplementation of elderly patients with protein between meals to prevent supplementation from replacing calories and nutrients consumed during regular meals (Fiatarone 1994).

The current information on whether to combine protein with carbohydrates requires further research before conclusions can be drawn. Studies on patients assigned to bed-rest have shown that a mixed meal of 16.5g of EAA with 30g of carbohydrates reduced muscle loss, with controls having a more pronounced loss of muscles strength (Paddon-Jones 2004). Volpi and colleagues concluded that combining a protein bolous with carbohydrates impaired protein synthesis in elderly subjects compared to a protein bolus alone (Volpi 2000). Reviews on the subject have concluded that the presence of carbohydrates in modest doses (<30g) do not impair muscle protein synthesis in the elderly however larger doses may negatively influence insulin levels and lower protein synthesis (Kim 2010, Koopman 2011).

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Differing protein sources and amino acid ratios produce varying results, illustrating the need for attention and detail when prescribing protein supplements to this population. Protein sources vary in the relative percentages of EAA as well as the speed at which they are digested and increase plasma levels. Whey protein isolates have shown benefit over casein protein mixtures in both the rate of availability of EAA in plasma and in the ability to stimulate protein synthesis in muscle cells (Pennings 2011). However, in a second 2011 study, Dideriksen et al showed no difference in muscle protein synthesis between whey and caseinate ingested after resistance training in the elderly (Dideriksen 2011).

Current evidence shows that animal protein improves lean muscle tissue better than vegetarian sourced protein (Pannemans 1998) and that amino acid supplements containing only essential amino acids (EAA) confer better results than mixed, or non-EAA supplements. A small trial looked at the administration of an EAA only meal to healthy older adults who do not perform exercise on a regular basis (Volpi 2003). Although the size of the trial is a significant limitation, the results clearly indicated that a meal containing 18g of EAA stimulated muscle protein synthesis to the same degree as a 40g meal containing 18g of EAA and 22g of non-essential amino acids.

Of greatest interest, leucine, a branched chain EAA, appears to regulate protein synthesis via multiple processes. Nicastro et al concluded in a 2011 review that leucine stimulates insulin release and is a regulatory molecule for skeletal muscle protein synthesis. Leucine also appears to influence cellular proteolytic processes, which may slow muscle loss (Nicastro 2011). Human controlled trials have shown that leucine enriched meals can improve muscle protein synthesis in the elderly at a dose of 2.8g of leucine in a mixed EAA meal (Katsanos 2006, Paddon-Jones 2004b). There are currently no dose-response trials on leucine supplementation, however the Katsanos trial (Katsanos 2006) was a follow up to a previous study (Katsanos 2005) that found that 1.7g of leucine did not stimulate protein synthesis in elderly subjects compared to younger controls when delivered in a 6.7g mixed protein meal. This possibly indicates a decrease in leucine sensitivity in the elderly with a threshold dose of approximately 2.8g needed to stimulate anabolism. The apparent decrease in leucine sensitivity may be due to age related alterations in first pass metabolism of leucine and other essential amino acids demonstrated by Volpi et al (Volpi 1999).

Much of the research on the adverse outcomes of leucine supplementation has been derived from animal models. The research on possible adverse effects, which include appetite suppression (Nicastro 2011) and imbalances in other branched chain amino acids (Verhoeven 2009) should be considered with caution given the differing needs in individual amino acids from humans to rats and the relatively low dosage of leucine needed in humans to cause a response in skeletal muscle (Nicastro 2011). Trappe et al reported no adverse effects after the administration of 3.6g of leucine in combination with other branched chain amino acids after 60 days (Trappe 2008) to prevent muscle loss during bedrest. In addition, a review by Fernstrom (Fernstrom 2005) found no reported adverse outcomes for supra-physiologic doses of branched chain amino acids in over 20 trials.

The timing of protein intake with respect to resistance exercise has been suggested as a possible treatment option to increase amino acid incorporation into skeletal muscle. In 2011, Pennings et al demonstrated for the first time that de novo protein synthesis is increased in elderly patients who combine protein and exercise versus protein ingestion alone. Subjects completed 30 minutes of stationary bike plus 2 leg resistance exercise before consuming 20g of protein (Pennings 2011b). Although the mechanism behind sarcopenia was thought to include anabolic resistance to exercise, studies have started to show that protein synthesis is increased in the elderly when protein and carbohydrates are ingested following exercise (Koopman 2008), and that the effect of protein ingestion, is delayed, not absent, when compared to younger controls (Drummond 2008).

In a 2011 study by Symons, the discrepancies in the research on the topic of protein and exercise are adequately addressed. In this study, participants were given a large dose of protein (90g) in an intact meal of lean ground beef 60 minutes before exercise. This resulted in a 108% increase in protein synthesis in elderly patients as well as younger controls (Symons 2011). It appears that the timing of protein ingestion should vary, depending on whether patients are consuming intact protein meals (beef, poultry) or quickly digested protein isolates or EAA only supplements. Full meals containing protein require up to 100 minutes to reach peak plasma levels, while protein supplements may elevate plasma AA levels in as little as 15-30 minutes. Timing of exercise and protein prescriptions are thus dependent on the type of protein ingested with intact meals consumed 60 minutes prior to exercise and protein supplements

in a 30-60 minute window post exercise (Symons 2011). Negative studies on protein and exercise have shown no additional benefit to adding exercise to protein intake but either have included subjects who consume >1.0g/kg/d of protein on a regular basis or have used large doses or protein, EAA or leucine over longer periods of time (Koopman 2008, Koopman 2011, Verdijk 2009). This research may suggest that the timing of protein intake with respect to exercise is most valuable as a treatment option in elderly patients who do not consume adequate protein at presentation, but that the benefits of timed doses cease as protein adequacy is reached.

Very few studies have examined protein intake and functional endpoints such as strength. It appears that protein intake is more closely linked to the prevention of appendicular lean mass than muscle strength however more studies are needed to confirm these findings (Scott 2010). One uncontrolled trial examined the use of an EAA+argenine mixture containing 3.95g of leucine and 1.10g of argenine on functional endpoints such as gait speed and maximal leg strength. The study employed only 12 participants but showed significant gains in muscle mass and all functional endpoints measured (Borsheim 2008).

The understanding of sarcopenia will undoubtedly continue to evolve, as already, the use of the term anabolic resistance has begun to shift to account for new research. Recent evidence shows that elderly patients respond to exercise as well as younger controls (Pennings 2011b, Symons 2011) and that the elderly respond similarly to the young after an EAA bolous that exceeds normal dietary intakes (Volpi 1999). It is clear that protein adequacy with a focus on EAA and leucine can prevent muscle wasting and restore muscle mass. Further research into the benefits of protein and sarcopenia are required to determine the effects of carbohydrates and exercise on protein synthesis and functional endpoints such as muscle strength. Sarcopenia is present in the majority of elderly patients and is a condition that can be prevented and possibly treated with careful, specific treatment planning including protein supplementation.

References

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Brass EP, Sietsema KE. Considerations in the development of drugs to treat sarcopenia. J Am Geriatr Soc. 2011 Mar;59(3):530-5.

Dideriksen KJ, Reitelseder S, Petersen SG, Hjort M, Helmark IC, Kjaer M, Holm L. Stimulation of muscle protein synthesis by whey and caseinate ingestion after resistance exercise in elderly individuals. Scand J Med Sci Sports. 2011 Apr 28.

Drummond MJ, Dreyer HC, Pennings B, Fry CS, Dhanani S, Dillon EL, Sheffield- Moore M, Volpi E, Rasmussen BB. Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging. J Appl Physiol. 2008 May;104(5):1452-61.

Fernstrom JD. Branched-chain amino acids and brain function. J Nutr. 2005 Jun;135(6 Suppl):1539S-46S.

Fiatarone MA, O’Neill EF, Ryan ND, Clements KM, Solares GR, Nelson ME, Roberts SB, Kehayias JJ, Lipsitz LA, Evans WJ. Exercise training and nutritional supplementation for physical frailty in very elderly people. N Engl J Med. 1994 Jun 23;330(25):1769-75.

Gallagher D, Ruts E, Visser M, Heshka S, Baumgartner RN, Wang J, Pierson RN, Pi-Sunyer FX, Heymsfi eld SB. Weight stability masks sarcopenia in elderly men and women. Am J Physiol Endocrinol Metab. 2000 Aug;279(2):E366-75.

Genaro Pde S, Martini LA. Effect of protein intake on bone and muscle mass in the elderly. Nutr Rev. 2010 Oct;68(10):616-23.

Houston DK, Nicklas BJ, Ding J, Harris TB, Tylavsky FA, Newman AB, Lee JS, Sahyoun NR, Visser M, Kritchevsky SB; Health ABC Study. Dietary protein intake is associated with lean mass change in older, community-dwelling adults: the Health, Aging, and Body Composition (Health ABC) Study. Am J Clin Nutr. 2008 Jan;87(1):150-5.

Katsanos CS, Kobayashi H, Sheffi eld-Moore M, Aarsland A, Wolfe RR. Aging is associated with diminished accretion of muscle proteins after the ingestion of a small bolus of essential amino acids. Am J Clin Nutr. 2005 Nov;82(5):1065-73.

Katsanos CS, Kobayashi H, Sheffi eld-Moore M, Aarsland A, Wolfe RR. A high proportion of leucine is required for optimal stimulation of the rate of muscle protein synthesis by essential amino acids in the elderly. Am J Physiol Endocrinol Metab. 2006 Aug;291(2):E381-7.

Kerstetter JE, O’Brien KO, Insogna KL. Low protein intake: the impact on calcium and bone homeostasis in humans. J Nutr. 2003 Mar;133(3):855S-861S.

Kim JS, Wilson JM, Lee SR. Dietary implications on mechanisms of sarcopenia: roles of protein, amino acids and antioxidants. J Nutr Biochem. 2010 Jan;21(1):1-13.

Koopman R. Dietary protein and exercise training in ageing. Proc Nutr Soc. 2011 Feb;70(1):104-13.

Koopman R, Verdijk LB, Beelen M, Gorselink M, Kruseman AN, Wagenmakers AJ, Kuipers H, van Loon LJ. Co-ingestion of leucine with protein does not further augment post-exercise muscle protein synthesis rates in elderly men. Br J Nutr. 2008 Mar;99(3):571-80.

Milne AC, Potter J, Vivanti A, Avenell A. Protein and energy supplementation in elderly people at risk from malnutrition. Cochrane Database Syst Rev. 2009 Apr 15;(2):CD003288.

Morley JE, Argiles JM, Evans WJ, Bhasin S, Cella D, Deutz NE, Doehner W, Fearon KC, Ferrucci L, Hellerstein MK, Kalantar-Zadeh K, Lochs H, MacDonald N, Mulligan K, Muscaritoli M, Ponikowski P, Posthauer ME, Rossi Fanelli F, Schambelan M, Schols AM, Schuster MW, Anker SD; Society for Sarcopenia, Cachexia, and Wasting Disease. Nutritional recommendations for the management of sarcopenia. J Am Med Dir Assoc. 2010 Jul;11(6):391-6.

Nicastro H, Artioli GG, Costa Ados S, Solis MY, da Luz CR, Blachier F, Lancha AH Jr. An overview of the therapeutic effects of leucine supplementation on skeletal muscle under atrophic conditions. Amino Acids. 2011 Feb;40(2):287-300.

Paddon-Jones D, Sheffeild-Moore M, Urban R, Sanford A, Aarsland A, Wolfe R, Ferrando A. Essential Amino Acid and Carbohydrate Supplmentation Ameliorates Muscle Protein Loss in Humans During 28 Days Bedrest. The Journal of Clinical Endorinology and Metabolism. 2004 89(9):4351-4358.

Paddon-Jones D, Sheffi eld-Moore M, Zhang XJ, Volpi E, Wolf SE, Aarsland A, Ferrando AA, Wolfe RR. Amino acid ingestion improves muscle protein synthesis in the young and elderly. Am J Physiol Endocrinol Metab. 2004b Mar;286(3):E321-8.

Pannemans DL, Wagenmakers AJ, Westerterp KR, Schaafsma G, Halliday D. Effect of protein source and quantity on protein metabolism in elderly women. Am J Clin Nutr. 1998 Dec;68(6):1228-35.

Pennings B, Boirie Y, Senden JM, Gijsen AP, Kuipers H, van Loon LJ. Whey protein stimulates postprandial muscle protein accretion more effectively than do casein and casein hydrolysate in older men. Am J Clin Nutr. 2011 May;93(5):997-1005.

Pennings B, Koopman R, Beelen M, Senden JM, Saris WH, van Loon LJ. Exercising before protein intake allows for greater use of dietary protein-derived amino acids for de novo muscle protein synthesis in both young and elderly men. Am J Clin Nutr. 2011b Feb;93(2):322-31.

Rolland Y, Dupuy C, Abellan van Kan G, Gillette S, Vellas B. Treatment strategies for sarcopenia and frailty. Med Clin North Am. 2011 May;95(3):427-38, ix.

Rousset S, Patureau Mirand P, Brandolini M, Martin JF, Boirie Y. Daily protein intakes and eating patterns in young and elderly French. Br J Nutr. 2003 Dec;90(6):1107-15.

Scott D, Blizzard L, Fell J, Giles G, Jones G. Associations between dietary nutrient intake and muscle mass and strength in community-dwelling older adults: the Tasmanian Older Adult Cohort Study. J Am Geriatr Soc. 2010 Nov;58(11):2129-34.

Solerte SB, Fioravanti M, Locatelli E, Bonacasa R, Zamboni M, Basso C, Mazzoleni A, Mansi V, Geroutis N, Gazzaruso C. Improvement of blood glucose control and insulin sensitivity during a long-term (60 weeks) randomized study with amino acid dietary supplements in elderly subjects with type 2 diabetes mellitus. Am J Cardiol. 2008 Jun 2;101(11A):82E-88E.

Symons TB, Sheffi eld-Moore M, Mamerow MM, Wolfe RR, Paddon-Jones D. The anabolic response to resistance exercise and a protein-rich meal is not diminished by age. J Nutr Health Aging. 2011 May;15(5):376-81.

Symons TB, Sheffi eld-Moore M, Wolfe RR, Paddon-Jones D. A moderate serving of high-quality protein maximally stimulates skeletal muscle protein synthesis in young and elderly subjects. J Am Diet Assoc. 2009 Sep;109(9):1582-6.

Trappe S, Creer A, Minchev K, Slivka D, Louis E, Luden N, Trappe T. Human soleus single muscle fi ber function with exercise or nutrition countermeasures during 60 days of bed rest. Am J Physiol Regul Integr Comp Physiol. 2008 Mar;294(3):R939-47.

Trappe TA, Carroll CC, Dickinson JM, LeMoine JK, Haus JM, Sullivan BE, Lee JD, Jemiolo B, Weinheimer EM, Hollon CJ. Infl uence of acetaminophen and ibuprofen on skeletal muscle adaptations to resistance exercise in older adults. Am J Physiol Regul Integr Comp Physiol. 2011 Mar;300(3):R655-62.

Trappe TA, White F, Lambert CP, Cesar D, Hellerstein M, Evans WJ. Effect of ibuprofen and acetaminophen on postexercise muscle protein synthesis. Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E551-6.

Verdijk LB, Jonkers RA, Gleeson BG, Beelen M, Meijer K, Savelberg HH, Wodzig WK, Dendale P, van Loon LJ. Protein supplementation before and after exercise does not further augment skeletal muscle hypertrophy after resistance training in elderly men. Am J Clin Nutr. 2009 Feb;89(2):608-16.

Verhoeven S, Vanschoonbeek K, Verdijk LB, Koopman R, Wodzig WK, Dendale P, van Loon LJ. Long-term leucine supplementation does not increase muscle mass or strength in healthy elderly men. Am J Clin Nutr. 2009 May;89(5):1468-75.

Vinciguerra M, Musaro A, Rosenthal N. Regulation of muscle atrophy in aging and disease. Adv Exp Med Biol. 2010;694:211-33.

Volpi E, Kobayashi H, Sheffi eld-Moore M, Mittendorfer B, Wolfe RR. Essential amino acids are primarily responsible for the amino acid stimulation of muscle protein anabolism in healthy elderly adults. Am J Clin Nutr. 2003 Aug;78(2):250-8.

Volpi E, Mittendorfer B, Rasmussen BB, Wolfe RR. The response of muscle protein anabolism to combined hyperaminoacidemia and glucose-induced hyperinsulinemia is impaired in the elderly. J Clin Endocrinol Metab. 2000 Dec;85(12):4481-90.

Volpi E, Mittendorfer B, Wolf SE, Wolfe RR. Oral amino acids stimulate muscle protein anabolism in the elderly despite higher fi rst-pass splanchnic extraction. Am J Physiol. 1999 Sep;277(3 Pt 1):E513-20.

Dr Ben Boucher,MD

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Dr Ben Boucher,MD

Integrative management of vector – transmitted illness

Dr Ben Boucher, MD, was born and raised in the Havre Boucher region (Antigonish County) of Nova Scotia. He is quick to highlight his Aboriginal and Acadian ancestry, which he traces back to the 1700’s, as a driving force in his lifelong self- image of individualism- an individual who finds himself having spent a lifetime at odds with the status quo. Physicians who fully embrace the tenants of individualized, holistic medicine seem to share this sense of “being different”, and Dr Boucher is no exception.

Every healthcare provider tells a story of when in their lives they felt compelled to pursue their respective career path. Ben describes his choice was made at the age of five, when he was called upon by his father to tend to an ailing relative. His formal training began in 1974 at Dalhousie Medical School, preceded by an honours undergraduate degree in biology from St Francis Xavier University. His interest in integrative medicine was established by the time he arrived at medical school. Ben described his medical training as “frustrating”, with “excessive competitiveness”, and a lack of interest in anything outside of established norms. He discussed a paper in his second year of medical school that assimilated evidence of vascular outcomes associated with vitamin E supplementation, and experienced scrutiny from professors for his efforts.

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He opened his first practice on Cape Breton Island in 1979, where he spent a wonderful summer working as the Warden for the Cape Breton Highlands National Park. He had a strong desire to “be where he was needed”, and Cape Breton seemed a perfect fit as the family physician of the community had passed away in 1949. Eventually Ben moved his practice to Port Hawksbury where he has been for the past 17 years.

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An extremely influential experience in Ben’s life occurred in 1990 when he attended an ACAM conference and chelation workshop. He was fascinated to learn concepts of oxidant/ antioxidant chemistry, the impact of heavy metals on human health, and the ability of chelation therapy to effectively treat vascular disease. He quickly implemented chelation therapy in his private practice, and since 2007 has served as a site for the ongoing TACT trial of chelation therapy for secondary prevention of cardiovascular disease. Shortly after implementing chelation therapy in private practice, Ben witnessed the therapy spare an elderly patient from amputation of a limb deemed necessary as a complication of diabetes.

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In 1991, three months after offering patients chelation, and on the heels of the one incredible case described above, the Provincial Medical Board of Nova Scotia (PMBNS) banned chelation therapy for vascular disease. Ben found this puzzling as he was the only physician in Nova Scotia offering the therapy at the time. Ben set into motion a cleaver series of events; the patient who had been spared from amputation and continued to receive regular chelation treatments had an attorney write the PMBNS and threaten to sue. The letter read to the effect of: “the treatment has been effective for me, has spared me amputation, and your actions threaten to make the treatment unavailable”. The PMBNS did not question future treatments.

In 2008 Ben began treating Lyme related illness. Again, the impetus stemmed from a desire to do what was needed. He no longer considers the paradigm as Lyme- related, preferring to apply a broader term he has coined; “vector transmitted infection”. While most public health effort in the area focuses on Lyme, Ben is quick to highlight a long list of vectors capable of transmitting illness, including bartonella, babesia, erlichia, anaplasma, and others. The basis for the present lack of understanding of these infections, and the poor definitions of treatment strategies primarily stem from the extreme difficulty in making an objective diagnosis. Sensitivity and specificity of testing methods, especially in cases where the infection is months to years old, are horrifically poor. To overcome this obstacle, Ben relies primarily on the patient’s symptomatic presentation to base the diagnosis.

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Ben’s approach to diagnosis relies on a thorough review of symptoms questionnaire, where patients are requested to rank the severity of each symptom they report. Ben suspects vector transmitted illness when a patient reports multiple symptoms (15+) that span multiple body systems, and that are of a very severe magnitude. Objective evaluation has ruled out more commonly suspected causes, leaving vector transmitted illness as the most likely cause. Ben has set the bar very high to suspect such illness, evidenced by the extreme magnitude of debility patients present with to be considered for the diagnosis. The treatment approach is aggressive, and long term. Antibiotics are the mainstay, but true to Ben’s holistic application of healthcare, the implementation takes on unique characteristics. First and foremost, patients are counselled to improve diet quality, and as treatment progresses to adopt physical activity. Initially, herbal antibiotics take the place of prescriptions; Ben has found that prescription antibiotics work better when herbal antibiotics are used first for a period of a couple of months. He uses the Byron White and other herbal formulas, commonly observing symptom picture severity improve from scores of 8-9/10 to scores of 3-4/10 within a couple of months, but then the patient plateaus. Prescription antibiotics are then introduced to “finish the job”, which again often requires several months of therapy to achieve.

Ben is eager to share his experiences in the realm of vector transmitted infections due to what he describes as an unacceptable negligence of the commonality of the problem. He sees himself as one of only a handful of physicians across Canada treating patients for this underlying cause of significant debility. As such, patients are referred to his care from across Canada.

As impressive as Ben’s achievements as a physician is his commitment to his community and his own health. Ben ran for political office in two separate elections during the 1980’s as an NDP candidate. He envisioned utilizing the web as a means of operating elections and national referendums, a strategy he felt would achieve greater involvement from the public in the process of politics, and reduce public apathy. As a patient role model, Ben lives the life he requests patients to follow, most evident in his personal fitness regime that includes pedal biking, swimming, kayaking, snow shoeing, and power walking.

IHP is grateful to Dr Ben Boucher for allowing us to present his work to you. He is a member of the rare club of physicians who have been blazing a path for future waves of integrative healthcare providers to follow long before the concepts were household in nature. He does not treat what is most convenient, but what is most pressing. In recent years he has found himself operating in an obscure field of medicine; instead of being intimidated in this arena of poor objective evaluation, his tireless efforts have produced the standard of care for it.

Halifax Naturopathic Health Centre

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Halifax Naturopathic Health Centre

A centre of excellence

The Halifax Naturopathic Health Centre opened its doors not even 18 months ago, yet it has seen itself swell to a facility boasting up to 250 patient visits per week, and has already fostered impressive referral networks with physicians across the province of Nova Scotia and across North America. The vision of two driven and passionate ND’s, Craig Herrington and Rosalyn Hayman, the Halifax Naturopathic Health Centre embodies the true essence of a modern facility of world class, evidence- based integrative healthcare that has caught the eye of the entire province

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The clinic’s founders set out with a series of clearly defined goals. They wanted to be the largest naturopathic facility in the province, and they successfully achieved this in the epicentre of the city of Halifax. They recognized the need for respectability and sought to bring on board a well- tenured local naturopathic physician to help achieve this; Dr Sarah Baillie, ND was inspired by the teams vision and joined the team in time for its opening, an ND who had been practicing in Halifax since 1999. The team demanded of itself delivery of best medical practices, choosing to implement evidence- based approaches afforded to the naturopathic profession. Eloquently executed marketing initiatives and professional networking programs quickly allowed the team to achieve its vision of a naturopathic facility integrated into the community and working hand- in- hand with an array of local conventional physicians.

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The facility has five treatment rooms, a blood lab, and an IV room. Jackie Batog, RN, has joined the team and manages all blood and injection services. Jackie runs all conventional and integrative diagnostic tests, performs injections, and sets up IV’s. The facility also boasts a highly diverse dispensary. Like many of the most successful clinics IHP interviews, the team carries a small number of items from each of a very large number of companies, as opposed to relying on two or three companies to stock their dispensary. “The best each company has to offer” governs the manner in which the dispensary is built. St Francis Herb Farm and Naturally Nova Scotia are the two botanical companies called upon to supply tinctures. NFH, Thorne, Cytomatrix, and a selection of Halifax Naturopathic Health Centre private label offerings comprise the nutraceutical companies most heavily relied upon.

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The facility is truly eclectic in terms of the types of patients attracted. It has established an excellent reputation in terms of cancer care, with physicians from across the city and province referring patients for this purpose. High dose vitamin C, low dose naltrexone, and an anti cachexia drip are commonly employed treatments for cancer, in addition to intense dietary counseling and an assortment of orally administered essential nutrients, botanical medicines, nutraceutical and functional food interventions. The facility also boats well- developed programs for women’s health, endocrine abnormalities, weight loss, and others.

In addition to the cachexia drip, the facility has pioneered a fibromyalgia drip featuring B complex vitamins, vitamin C, MSM, and glutathione. For patients with chronic pain, neurotherapy and prolotherapy are commonly employed. Chelation therapy for cardiovascular disease is another important offering of the facility, utilizing EDTA and/ or plaquex (a phosphatidylcholine solution). Jackie Batog, RN, has introduced unique and cutting- edge diagnostic options, notably an advanced cardiovascular risk panel that includes assessment of Apo-E, LDL subclasses, oxidized LDL, etc…

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The team has effectively implemented a round table approach to patient care. Frequent meetings are held to review tough cases. An environment devoid of competition has successfully been created. Patients are frequently seen by multiple ND’s within the same facility, coinciding with the evolution of the specific case and the requirements of the next stage of care. The team has found that the minds of four ND’s working together deliver superior patient outcomes relative to what any one of the ND’s could achieve alone. Some simple themes emerge as the team describes what they perceive as the keys to the success of the Halifax Naturopathic Health Centre. Locating in an under-serviced area of Canada meant a population eager for effective holistic treatments was awaiting their arrival. A commitment to an evidencebased practice resonated well not only with patients but with surrounding conventional physicians the team intended on achieving collaboration with. A simple but well- executed marketing plan that included bringing an experienced and respected ND on board, networking with local physicians, and lectures to groups that included corporate seminars as well as a local women’s and children’s hospital.

IHP is grateful to the Halifax Naturopathic Health Centre for allowing us to showcase their work to you. Their diligence, hard work, and commitment to excellence in naturopathic medicine has allowed for a quick and impressive magnitude of integration with the surrounding community. Their decision to apply effort to integrate with local physicians has proven invaluable. The number of conventional physicians open to sound delivery of integrative medicine is growing at an exponential pace. We wish the team continued success in delivering an exceptional standard of care to an under- serviced region of the country.

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Sodium and risk of death: Villain or biomarker?

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Sodium and risk of death: Villain or biomarker?

Introduction A large body of evidence has linked higher intake of sodium with increased risk of chronic disease, most notably stroke and cardiovascular disease, and all cause death (Yang 2011). In recognition of this association, many initiatives have been launched globally to reduce dietary sodium intake most notably though the reduction of sodium content of processed foods (Henney 2010, van Vliet 2011, Webster 2011). This article examines the evidence around sodium as a risk factor for cardiovascular disease and death, drawing on lessons learned from the beta carotene experience.

In Europe, the current leader in sodium reduction initiatives, national programs have been launched in 19 countries, with reductions of up to 25% in sodium content of key foods, yielding reductions of approximately 1-3 g per day in per capita sodium intake (from a baseline of between 8-12 g per day) (Webster 2011). This has been paralleled by documented reductions of up to 60-80% in coronary artery disease and stroke mortality in Finland and Japan respectively: Finland launched a comprehensive cardiovascular disease prevention program in the 1970s and experienced a 65% decrease in cardiovascular mortality by 1995 (He 2009, Laatikainen 2006, Puska 1998, Webster 2011). Likewise, according to the World Action on Salt and Health organization, Japan documented an 80% reduction in mortality in the wake of its salt reduction program (Iso 1999, WASH).

Currently, sodium recommendations for healthy individuals (adequate intake) in Canada and the US are 1500 mg per day (van Vliet 2011), with a tolerable upper limit of 2300 mg (Henney 2010), based on reference values set by the Institute of Medicine in 2005 (Henney 2010). The American Heart Association further recommends a limit of no more than 1500 mg per day (AHA 2011). Actual average daily intake during 2003–2006, estimated by the Institute of Medicine, was 3,614 mg/d (Henney 2010).

Sodium and Risk of Death: Observational Evidence

NHANES III, the third National Health and Nutrition Examination Survey (1988-2006) was a prospective cohort study of a nationally representative sample of US adults; Yang et al studied data from a subset of 12,267 subjects with available data for associations between sodium intake and mortality from all-causes, cardiovascular, and ischemic heart (IHD) disease (2011). Higher sodium intake was associated with significantly increased risk of all-cause mortality, hazard ratio HR 1.20 (95% confidence interval CI 1.03-1.41 per every 1000 mg/d increase), whereas higher potassium intake was associated with lower mortality risk (HR 0.80, 95% CI 0.67-0.94 per 1000 mg/d).

Furthermore, those in the highest quartile sodium-potassium intake ratio compared to the lowest quartile also had significantly elevated risk: HR 1.46 (95% CI 1.27-1.67) for all-cause mortality; HR 1.46 (95% CI 1.11-1.92) for CVD mortality; and HR 2.15 (95% CI 1.48-3.12) for IHD mortality.

Similar findings were reported based on data from the first NHANES study (He 1999). A total of 14,407 subjects were included, and dietary sodium and energy intake were estimated at baseline using a single 24-hour dietary recall method. Among overweight persons with an average energy intake of 7452 kJ (~1781 calories), a 100 mmol higher sodium intake was associated with a 32% increase (relative risk RR 1.32, 95% CI 1.07-1.64, P = .01) in stroke incidence; an 89% increase (RR 1.89, 95% CI 1.31-2.74, P<.001) in stroke mortality; a 61% increase (RR 1.61, 95% CI 1.32-1.96, P<.001) in cardiovascular disease mortality; and a 39% increase (RR 1.39, 95% CI, 1.23-1.58, P<.001) in mortality from all causes. However, in this study dietary sodium intake was not significantly associated with cardiovascular disease risk in non-overweight persons.

Such studies have also been conducted in Japan. Nagata et al (2004) investigated sodium intake and risk of death from stroke among 13,355 men and 15 724 women in Takayama City, Japan. In men, the highest compared with the lowest tertile of sodium intake was significantly positively associated with death from stroke (total from ischemic and hemorrhagic) after controlling for covariates, HR 2.33 ( 95% CI 1.23 -4.45). Significant positive associations were also observed between sodium intake and death from ischemic stroke (HR 3.22, 95% CI 1.22-8.53) as well as death from intracerebral hemorrhage (HR 3.85, 95% CI 1.16 -12.7). In women, a non significant association between sodium intake and death from stroke was found : HR 1.70, 95% CI, 0.96 -3.02 and HR 2.10, 95% CI 0.96 – 4.62, respectively.

Takachi et al (2010) investigated the relationship between consumption of sodium and cancer and cardiovascular disease. Between 1995-1998, a total of 77,500 men and women aged 45-74 years were enrolled, and followed until the end of 2004; 4476 cases of cancer and 2066 cases of cardiovascular disease (CVD) were identified. Results showed that higher consumption of sodium was associated with a higher risk of CVD but not with the risk of total cancer: multivariate HR for the highest compared with lowest quintiles of intake were 1.19 (95% CI 1.01-1.40; P trend 0.06) for CVD and 1.04 (95% CI 0.93-1.16; P trend: 0.63) for total cancer.

Umesawa et al (Umesawa 2008) report a Japanese population study conducted between 1988 -1990 among 58,730 Japanese subjects aged 40-79 y with no history of stroke, coronary heart disease, or cancer. After 745,161 person-years of follow-up, 986 deaths from stroke (153 subarachnoid hemorrhages, 227 intraparenchymal hemorrhages, and 510 ischemic strokes) and 424 deaths from coronary heart disease were documented. Sodium intake was associated with mortality from total stroke, ischemic stroke, and total cardiovascular disease. The multivariable HR for the highest versus the lowest quintiles of sodium intake after adjustment for age, sex, and cardiovascular disease risk factors was 1.55 (95% CI 1.21- 2.00; P trend < 0.001) for total stroke; 2.04 (95% CI 1.41- 2.94; P for trend < 0.001) for ischemic stroke; and 1.42 (95% CI 1.20- 1.69; P for trend < 0.001) for total cardiovascular disease. As with NHANES III, this study also found an inverse relationship between potassium intake and risk of death.

Strazzullo et al conducted a meta-analysis of 19 prospective cohorts examining the association between sodium intake and risk of stroke or cardiovascular disease (2009). The analysis included 177,025 participants with follow-up between 3.5-19 years, and over 11,000 vascular events. Higher salt intake was associated with increased risk of stroke (relative risk RR 1.23, 95% CI 1.06 -1.43; P=0.007) and cardiovascular disease (1.14, 0.99 – 1.32; P=0.07). For cardiovascular disease, sensitivity analysis showed that the exclusion of a single study led to a significant result: RR 1.17 (1.02 – 1.34; P=0.02). The associations observed were greater the larger the difference in sodium intake and the longer the follow-up. The authors concluded: “high salt intake is associated with significantly increased risk of stroke and total cardiovascular disease. Because of imprecision in measurement of salt intake, these effect sizes are likely to be underestimated. These results support the role of a substantial population reduction in salt intake for the prevention of cardiovascular disease.”

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The Beta Carotene Experience: A Harsh Lesson Learned in the Concept of Biomarker With the emergence of well- constructed theories of the role of oxidant stress in the initiation of atherosclerosis (Ross 1993) and cancer (Cerutti 1991) came an explosion of research into the potential for a handful of antioxidant nutrients to prevent and treat “the big two” chronic degenerative diseases. The landmark Basel study for many confirmed suspicions of the powerful ability of antioxidants to prevent such diseases; in an observational cohort of 4858 men followed for 12 years, Basel researchers found individuals in the lowest quintile of plasma beta carotene were at a 60% increased risk of developing cancer relative to individuals in the highest quintile of plasma beta carotene (Stahelin 1991). The stage was set for large, multicentre, randomized control trials of intervention with antioxidant nutrients for the prevention and treatment of heart disease and cancer.

An understatement is to call the outcomes of these intervention trials “disappointing”. Cochrane recently summarized 67 trials of antioxidant nutrients with 232,550 participants collectively (Bjelakovic 2008). The reviewers found a 16% increased risk in all cause death from vitamin A supplementation (RR 1.16, 95% CI 1.10 to 1.24), a 7% increased risk in all cause death from beta carotene supplementation (RR 1.07, 95% CI 1.02-1.11), and a 4% increased risk in all cause death from vitamin E supplementation (RR 1.04, 95% CI 0.94-1.20).

The mechanistic basis upon which oxidant stress contributes to initiation and progression of heart disease and cancer remains sound. So what accounts for the lack of benefit, and marked detriment, from intervention with this selection of antioxidant nutrients?

The concept of biomarker was quickly identified. Plasma determination of any one antioxidant nutrient does a poor job of providing insight into the biological impact of that specific nutrient. Instead, plasma determination of an antioxidant serves as an accurate biomarker of exposure to fruit and vegetables. The collective conscious of nutritional scientists was quick to incorporate this important fact in interpretation of relevant evidence moving forward, and what has emerged is a new era of research into whole foods and intervention trials focused on diet modification as opposed to single nutrient intervention

Modern trials that intervene with diet counseling have come to rely on plasma determination of beta carotene for an important task; serving as an accurate marker of fruit and vegetable intake, assessment of plasma beta carotene objectively confirms compliance or lack thereof with diet instructions of the trial. A simple example is the use of beta carotene assessment by WHEL investigators, an intervention trial in 3088 breast cancer survivors with a mean follow- up of 7.3 years examining the impact of diet and lifestyle counseling on cancer- free survival, invasive breast cancer events, and all cause mortality (Pierce 2007).

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Is Sodium a Biomarker?

Very little sodium occurs naturally in foods, and it is widely recognized that processed foods are the major source of sodium in the Standard American Diet (SAD). In addition to sodium chloride, table salt, sodium may be added to food as the flavour enhancer monosodium glutamate, sodium benzoate, sodium bicarbonate, sodium citrate, sodium nitrite, and sodium acid pyrophosphate (Fischer 2009). The Canadian Stroke Network’s website www.sodium101.ca states that over 70% of dietary sodium comes from processed foods (Figure 1).

Table 1. Sodium content of processed versus non-processed foods
Table 1. Sodium content of processed versus non-processed foods

In view of the beta carotene experience, the undeniable link between sodium intake and risk of death, and the fact that upwards of 70% of dietary sodium originates from processed foods, we posit that sodium intake may in fact function as a biomarker of the effect of processed foods. Since processed foods represent by far the predominant source of dietary sodium, the link between sodium intake and risk of death in these population studies may actually represent the relationship between intake of processed foods and death/ disease. Besides sodium, processed foods contain several other harmful substances such as nitrates, saturated and trans fats, (sodium) benzoate, MSG, many other preservatives and flavoring agents, as well as possible byproducts of processing that are as yet unidentified. Processed foods are also typically quite calorie-dense, thus promoting obesity and its health consequences. Furthermore, high intake of processed foods is typically accompanied by low intake of fruit and vegetables, the primary source of dietary potassium, and this may help explain the additional predictive power of sodium: potassium ratio and mortality, as shown in the studies cited above.

A recent Cochrane review examining the effect of intervention with low-sodium diets lends further support to this hypothesis (Taylor 2011). After pooling seven RCTs including 6489 participants with follow up of between seven months to 12.7 years, Taylor et al found no “strong benefit” from sodium restriction on mortality and cardiovascular morbidity (2011). Among patients who were normotensive, relative risk for all cause mortality at the end of the trial was RR 0.67 (95% CI 0.40-1.12, 60 deaths), and after the longest follow up, risk was RR 0.90 (95% CI 0.58-1.40, 79 deaths).

Among hypertensive subjects, risk at the end of trial was RR 0.97 (95% CI 0.83-1.13, 513 deaths), and after the longest follow up, risk was RR 0.96 (95% CI 0.83-1.11, 565 deaths) showing no strong evidence of any effect of salt reduction. Cardiovascular morbidity in people with normal blood pressure or raised blood pressure at baseline showed no strong evidence of benefit from salt restriction. Conversely, salt restriction increased the risk of all-cause death in those with congestive heart failure (end of trial RR 2.59, 95% 1.04-6.44, 21 deaths).

Taylor’s paper raised a great deal of controversy. He et al (2011) have argued that the pooled analysis had insufficient statistical power, and that this is the reason for null results. Nonetheless, it raises important questions as to the true role of sodium as an agent of cardiovascular disease.

Exceptions

Our hypothesis pertains to the population as a whole. We wish to point out that reduced sodium intake is a critical factor in a subset of hypertensive patients who are sodium-sensitive, as well as in patients with chronic renal disease.

Conclusion

There is a well- established link between dietary sodium intake and risk of death, in particular cardiovascular mortality. As illustrated by the beta carotene experience, however, sodium may function as a biomarker rather than as the causative agent. Since the major source of dietary sodium in the Standard American Diet is processed foods, measurement of sodium intake may actually reflect consumption of processed foods and the complex combination of food chemicals and/ byproducts contained therein. We suggest that sodium has been unfairly vilified as an agent of harm, and that in fact harm is due to the complex, disease-promoting constituents of processed foods.

References

AHA (American Heart Association). 2011 Dietary and Lifestyle Recommendations. Updated 2011. http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyDietGoals/Dictionary-of-Nutrition_UCM_305855_Article.jsp. Accessed 8 October 2011.

Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database Syst Rev. 2008 Apr 16;(2):CD007176.

Brown IJ, Tzoulaki I, Candeias V, Elliott P. Salt intakes around the world: implications for public health. Int J Epidemiol. 2009 Jun;38(3):791-813.

Cerutti PA, Trump BF. Inflammation and oxidative stress in carcinogenesis. Cancer Cells. 1991 Jan;3(1):1-7.

CDC (Center for Disease Control). Salt: Sodium and Food Sources. Updated 10 February 2010. http://www.cdc.gov/salt/food.htm Accessed 8 October 2011.

Fischer PW, Vigneault M, Huang R, Arvaniti K, Roach P. Sodium food sources in the Canadian diet. Appl Physiol Nutr Metab. 2009 Oct;34(5):884-92.

He J, Ogden LG, Vupputuri S, Bazzano LA, Loria C, Whelton PK. Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA. 1999 Dec 1;282(21):2027-34.

He FJ, MacGregor GA. A comprehensive review on salt and health and current experience of worldwide salt reduction programmes. J Hum Hypertens 2009; 23:363 – 384.

He FJ, MacGregor GA. Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials. Lancet. 2011 Jul 30;378(9789):380-2.

Institute of Medicine (US) Committee on Strategies to Reduce Sodium Intake; Henney JE, Taylor CL, Boon CS, editors. Strategies to Reduce Sodium Intake in the United States. Washington (DC): National Academies Press (US); 2010.

Iso H, Shimamoto T, Yokota K, Ohki M, Sankai T, Kudo M, Harada M, Wakabayashi Y, Inagawa M, Kitamura A, Sato S, Imano H, Iida M, Komachi Y. [Changes in 24-hour urinary excretion of sodium and potassium in a community-based heath education program on salt reduction]. Nihon Koshu Eisei Zasshi. 1999 Oct;46(10):894-903.

Laatikainen T, Pietinen P, Valsta L, Sundvall J, Reinivuo H, Tuomilehto J. Sodium in the Finnish diet: 20-year trends in urinary sodium excretion among the adult population. Eur J Clin Nutr 2006; 60:965 – 970.

Mattes, RD, Donnelly, D. Relative contributions of dietary sodium sources. Journal of the American College of Nutrition. 1991 Aug;10(4):383-393.

Nagata C, Takatsuka N, Shimizu N, Shimizu H. Sodium intake and risk of death from stroke in Japanese men and women. Stroke. 2004 Jul;35(7):1543-7.

Ni Mhurchu C, Capelin C, Dunford EK, Webster JL, Neal BC, Jebb SA. Sodium content of processed foods in the United Kingdom: analysis of 44,000 foods purchased by 21,000 households. Am J Clin Nutr. 2011 Mar;93(3):594-600.

Pierce JP, Natarajan L, Caan BJ, Parker BA, Greenberg ER, Flatt SW, Rock CL, Kealey S, Al-Delaimy WK, Bardwell WA, Carlson RW, Emond JA, Faerber S, Gold EB, Hajek RA, Hollenbach K, Jones LA, Karanja N, Madlensky L, Marshall J, Newman VA, Ritenbaugh C, Thomson CA, Wasserman L, Stefanick ML. Influence of a diet very high in vegetables, fruit, and fiber and low in fat on prognosis following treatment for breast cancer: the Women’s Healthy Eating and Living (WHEL) randomized trial. JAMA. 2007 Jul 18;298(3):289-98.

Puska P, Vartiainen E, Tuomilehto J, Salomaa V, Nissinen A. Changes in premature deaths in Finland: successful long-term prevention of cardiovascular diseases. Bull World Health Organization 1998; 76:419–425.

Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993 Apr 29;362(6423):801-9.

Stahelin HB, Gey KF, Eichholzer M, Ludin E, Bernasconi F, Thurneysen J, Brubacher G. Plasma antioxidant vitamins and subsequent cancer mortality in the 12-year follow-up of the prospective Basel Study. Am J Epidemiol. 1991 Apr 15;133(8):766-75.

Strazzullo P, D’Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ. 2009 Nov 24;339:b4567.

Takachi R, Inoue M, Shimazu T, Sasazuki S, Ishihara J, Sawada N, Yamaji T, Iwasaki M, Iso H, Tsubono Y, Tsugane S; Japan Public Health Center-based Prospective Study Group. Consumption of sodium and salted foods in relation to cancer and cardiovascular disease: the Japan Public Health Center-based Prospective Study. Am J Clin Nutr. 2010 Feb;91(2):456-64.

Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S. Reduced dietary salt for the prevention of cardiovascular disease. Cochrane Database Syst Rev. 2011 Jul 6;(7):CD009217.

Umesawa M, Iso H, Date C, Yamamoto A, Toyoshima H, Watanabe Y, Kikuchi S, Koizumi A, Kondo T, Inaba Y, Tanabe N, Tamakoshi A; JACC Study Group. Relations between dietary sodium and potassium intakes and mortality from cardiovascular disease: the Japan Collaborative Cohort Study for Evaluation of Cancer Risks. Am J Clin Nutr. 2008 Jul;88(1):195-202.

Van Vliet BN, Campbell NR; Canadian Hypertension Education Program. Efforts to reduce sodium intake in Canada: why, what, and when? Can J Cardiol. 2011 Jul-Aug;27(4):437-45.

Webster JL, Dunford EK, Hawkes C, Neal BC. Salt reduction initiatives around the world. J Hypertens. 2011 Jun;29(6):1043-50.

WASH (World Action on Salt and Health). Evidence: Population Studies http:// www.worldactiononsalt.com. Accessed 8 October 2011.

Yang Q, Liu T, Kuklina EV, Flanders WD, Hong Y, Gillespie C, Chang MH, Gwinn M, Dowling N, Khoury MJ, Hu FB. Sodium and potassium intake and mortality among US adults: prospective data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2011 Jul 11;171(13):1183-91. 078-

Serum phosphate levels are associated with aortic valve sclerosis and annular calcification

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Mineral metabolism disturbances are common among older people and may contribute to cardiac valvular calcification. The current study was conducted to evaluate mineral metabolism markers as potential risk factors for calcific aortic valve disease. Serum levels of phosphate, calcium, parathyroid hormone, and 25-hydroxyvitamin D were measured in 1938 Cardiovascular Health Study participants who were free of cardiovascular disease and who underwent echocardiographic measurements of aortic valve sclerosis (AVS), mitral annular calcification (MAC), and aortic annular calcification (AAC). The respective prevalences of AVS, MAC, and AAC were 54%, 39%, and 44%. Each 0.5 mg/dl higher serum phosphate concentration was associated with greater adjusted odds of AVS (odds ratio [OR]: 1.17, 95% confidence interval [CI]: 1.04 to 1.31, p = 0.01), MAC (OR: 1.12, 95% CI: 1.00 to 1.26, p = 0.05), and AAC (OR: 1.12, 95% CI: 0.99 to 1.25, p = 0.05). Serum calcium, parathyroid hormone, and 25-hydroxyvitamin D concentrations were not associated with aortic or mitral calcification. Therefore, phosphate may be a novel risk factor for calcific aortic valve disease as higher serum phosphate levels within the normal range were associated with valvular and annular calcification. J Am Coll Cardiol. 2011 Jul 12;58(3):291-7. PMID: 21737022.

Short sleep duration increases energy intake but not energy expenditure

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Evidence suggests that there is a relationship between short sleep duration and obesity so the current study assessed energy balance during periods of short and habitual sleep. Fifteen men and 15 women aged 30–49 years with a body mass index of 22–26 kg/m2 who regularly slept 7–9 hours/night participated in this crossover study. Participants were studied under short (4 hour/night) and habitual (9 hour/night) sleep conditions, in random order, for five nights each. Food intake was measured on day five, and energy expenditure was measured with the doubly labeled water method over each period. Participants consumed more energy on day five during short sleep than during habitual sleep (P = 0.023) and this effect was mostly due to increased consumption of fat (P = 0.01), notably saturated fat (P = 0.038). Resting metabolic rate and total energy expenditure did not differ significantly between sleep phases. These data show that a reduction in sleep increases energy and fat intakes, which may explain the associations observed between sleep and obesity. If sustained and not compensated by increased energy expenditure, the dietary intakes of individuals undergoing short sleep predispose to obesity. Am J Clin Nutr. 2011 Aug;94(2):410-6. PMID: 21715510.

Even low to moderate sugar-sweetened beverages impair glucose and lipid metabolism and promote inflammation

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The following prospective, randomized, controlled crossover study was conducted to investigate the effects of small to moderate consumption of sugar-sweetened beverages (SSBs) for three weeks on glucose and lipid metabolism, and inflammatory markers in 29 healthy young men. Six 3-week interventions were assigned in random order as 1) dietary advice to consume low amounts of fructose or 600 mL SSBs containing 2) medium fructose (MF): 40 g fructose/day); 3) high fructose (HF): 80 g fructose/day; 4) medium glucose (MG): 40 g glucose/day; 5) high glucose (HG): 80 g glucose/day; and 6) high sucrose (HS): 80 g sucrose/day. Results revealed that LDL particle size was reduced after HF and HS (P < 0.05 for both) and a more atherogenic LDL subclass distribution was seen with fructose-containing SSBs (P < 0.05). Fasting glucose and high-sensitivity C-reactive protein increased significantly after all interventions (by 4–9% and 60–109%, respectively; P < 0.05) and leptin increased during interventions with glucose-containing SSBs (MG and HG: P < 0.05). This study shows potentially harmful effects of low to moderate consumption of SSBs on markers of cardiovascular risk within just three weeks in healthy young men. Am J Clin Nutr. 2011 Aug;94(2):479-85. PMID: 21677052.

Dietary fructose may increase the risk of metabolic syndrome

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Excessive fructose intake may induce adverse metabolic effects but the effect of usual amounts of fructose intake on metabolic syndrome (MetS) is unknown. This cross-sectional population based study was conducted to determine the association of fructose intake and prevalence of MetS and its components. Subjects included 2537 participants of the Tehran Lipid and Glucose Study (45% men, aged 19-70 years). Dietary data were collected using a validated 168-item semi-quantitative food frequency questionnaire. Dietary fructose intake was calculated by sum of natural fructose in fruits and vegetables and added fructose in commercial foods. Mean total dietary fructose intakes were 46.5+/-24.5 and 37.3+/-24.2 grams/day in men and women, respectively. Compared with those in the lowest quartile of fructose intakes, men and women in the highest quartile, respectively, had 33% (95% CI, 1.15-1.47) and 20% (95% CI, 1.09-1.27) higher risk of MetS; 39% (CI, 1.16-1.63) and 20% (CI, 1.07-1.27) higher risk of abdominal obesity; 11% (CI, 1.02-1.17) and 9% (CI, 1.02-1.14) higher risk of hypertension; and 9% (CI, 1-1.15) and 9% (1.04-1.12) higher risk of impaired fasting glucose. The authors concluded that higher consumption of dietary fructose may have adverse metabolic effects. Nutr Metab (Lond). 2011 Jul 12;8(1):50. PMID: 21749680.

Cortisol, energy intake, and food frequency in overweight/obese women

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This retrospective study investigated the relationship between daily urinary free cortisol excretion rate (as a marker of cortisol production rate) and daily caloric intake, food choice, body mass index (BMI), and waist circumference. One hundred twenty-seven overweight/obese women and 21 normal-weight subjects were enrolled in the study. Cortisol excretion rate was assessed using a 24-hour urine collection (UFC/24 h). In obese patients, the daily caloric intake was calculated, and a weekly food-frequency questionnaire was assessed. Results revealed that obese women had significantly higher UFC/24 h than the normal-weight women (P < 0.001). The obese subjects had an unbalanced diet, particularly rich in saturated lipids, and weekly food choice showed a preference for highly caloric foods. UFC/24 h values and waist circumference were significantly correlated (P < 0.001), regardless of BMI. In the obese group, the UFC/24 h values were also significantly and positively correlated to daily carbohydrate and lipid intake and to weekly starchy food consumption even after adjustment for BMI. This study demonstrated a significant association between higher UFC/24 h and energy intake, fats, and consumption of starchy foods, and that these relations were independent of BMI. Nutrition. 2011 Jun;27(6):677-80. PMID: 20934852.

Iron deficiency in obesity is predicted by obesity-related inflammation rather than dietary iron intake

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Obese individuals may be at increased risk of iron deficiency (ID), but it is unclear whether this is due to poor dietary iron intakes or to adiposity-related inflammation. The current study investigated the relations between body mass index (BMI), dietary iron, iron status, and inflammation [C-reactive protein (CRP)]. Data from the 1999 Mexican Nutrition Survey, which included 1174 children and 621 nonpregnant women, were analyzed. The prevalence of ID was significantly higher in obese women and children compared with normal-weight subjects [odds ratios (95% CIs): 1.92 (1.23, 3.01) and 3.96 (1.34, 11.67) for women and children, respectively]. Despite similar dietary iron intakes in the two groups, serum iron concentrations were lower in obese women than in normal-weight women (P = 0.014) and total-iron-binding capacity was higher in obese children than in normal-weight children (P < 0. (provigil) 001). CRP concentrations in obese women and children were 4 times those of their normal-weight counterparts (P < 0.05) and CRP, but not iron intake, was a strong negative predictor of iron status (P < 0.05). The increased risk of ID in obesity may be due to the effects of obesity-related inflammation on dietary iron absorption. Am J Clin Nutr. 2011 May;93(5):975-83. PMID: 21411619.

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