Maandelijks archief: januari 2014

Kurkuma dood een tumorstamcel

Geplaatst op door
Posted on: 

Wednesday, January 29th 2014 at 7:45 am

Written By: 

Sayer Ji, Founder

Turmeric Extract Strikes To The Root Cause of Cancer Malignancy

A new turmeric study published in Cancer Letters is paving the way for a revolution in the way that we both understand and treat cancer. Titled, “Targeting cancer stem cells by curcumin and clinical applications,” U.S. researchers evaluated the primary polyphenol in the Indian spice known as curcumin for its ability to target cancer stem cells (CSCs), which are believed to be at the root cause of tumor formation and malignancy.

Whereas conventional models of cancer assumed that the majority of the cancer cells within a tumor possess self-renewal capacity to differing degrees, the CSC model proposes that, “[T]he initiation, maintenance, and growth of a tumor is driven by a minor population of cancer cells termed cancer stem cells (CSCs),” and that “These CSCs undergo continuous self-renewal and differentiate to heterogeneous cancer cells, yielding new tumors recapitulating the parental tumors, while the majority of cancer cells lack self-renewal capacity.”   

In other words, the CSCs are at the apex of a hierarchy of cells within the tumor, and are the “mother” of the various daughter cells that make it up, most of which are intrinsically benign. Conventional treatment with chemotherapy and radiotherapy, based on a rodent model with a 2-year experimental window to evaluate treatment efficacy and safety, was incapable of comprehending the CSC-mediated cause of post-treatment tumor recurrence, which in humans can take decades after initial treatment to manifest. Although it was possible to debulk a tumor with surgery, chemotherapy and radiation, CSC populations were often missed or even enriched as a result. When the tumor mass regrew it often became more invasive and treatment-resistant, resulting in the rapid demise and death of the patient — deaths which are often written off inaccurately or disingenuously as non-treatment related.

Given that conventional treatment can drive an intrinsically benign tumor (i.e., so-called indolent tumors) into greater invasiveness through increasing the number of intrinsically resilient cancer stem cells at the very same moment that it kills the less or non-harmful daughter cells, alternative treatment approaches are needed now more than ever.

The Cancer Stem Cell Killing Role of Turmeric (Curcumin)

Turmeric and curcumin extract have been extensively studied for their ability to kill various cancer cell lines. In fact, the literature is so abundant (see: 600 health benefits of turmeric) that it is both surprising and disheartening that so many patients who are in need of safe, effective and affordable treatments are not being given information about it. 

 

BECEL is niet goed voor hart en vaatziekten

Geplaatst op door

Ik herhaal het nog een keer… want de niet complementaire tak van voeding komt er geloof ik ook achter. Onverzadigde plantenvetten met omega-6 zijn Afbeeldingniet zo gezond als lange tijd gedacht werd. Een nieuwe analyse van oude data laat zien dat hartpatiënten die verzadigde (dierlijke) vetten door plantaardige onverzadigde vetten met omega-6-vetzuur vervangen een grotere kans hebben om te sterven aan hart- en vaatziekten.

Tot nu toe werd altijd aangenomen dat omega-6-vetzuur, waarvan linolzuur het bekendste is, een gunstig effect heeft op het cholesterolgehalte en daarmee op het risico op hart- en vaatziekten.

Controlegroep 

Een team van onderzoekers uit de VS en Australië heeft oude onderzoeksgegevens opnieuw geanalyseerd met moderne statistische methoden. Het gaat om een studie naar 458 hartpatiënten in Sydney die tussen 1966 en 1973 gevolgd werden.

De helft van de groep werd gevraagd een deel van de verzadigde vetten die ze consumeerden te vervangen door plantaardige onverzadigde vetten met omega-6 en linoolzuur. De andere helft van de groep deed dat niet. Uit de analyse bleek dat de omega-6-groep meer kans liep om te overlijden aan een hart- of vaatziekte dan de controlegroep.

Dieetadviezen 

De uitkomst van dit onderzoek werd ook naast de resultaten van andere studies gelegd. De conclusie van die meta-analyse was dat er geen bewijs bestaat dat omega-6-vetzuren goed zijn voor de gezondheid en dat ze mogelijk zelfs het risico verhogen op hart- en vaatziekten.

Volgens de onderzoekers kan deze conclusie grote gevolgen hebben voor dieetadviezen en gezondheidsaanbevelingen wereldwijd. Zo heeft de Amerikaanse Hartstichting onlangs nog de aanbeveling gedaan om meer omega-6-vetzuren te eten.

 

Obesitas

Geplaatst op door

Obesitas staat niet op zichzelf en gaat vaak samen met andere chronische ziekten en risicofactoren. Het Centraal Bureau voor de Statistiek ziet deze trend in haar cijfers.

Een op de tien Nederlanders had in 2012 ernstig overgewicht, oftewel een BMI hoger dan 30. Deze groep mensen heeft vaker te maken met diabetes, hypertensie, artrose, hart- en vaatziekten en psychische klachten, ziet het CBS. Het aandeel mensen met (ernstig) overgewicht neemt daarbij al jaren toe.

Om een voorbeeld te geven: ruim 13 procent van de mensen van 12 jaar of ouder met overgewicht heeft diabetes type 2. Bij dezelfde groep mensen met een gezond gewicht is dat veel lager, namelijk 1,5 procent. Hypertensie komt vier keer zo vaak voor bij mensen met obesitas.

Mensen met matig overgewicht, een BMI tussen de 25 en 30, hebben ook vaker met deze chronische ziekten en risicofactoren te maken, maar niet zo vaak als mensen met obesitas.

Het CBS heeft de cijfers gecorrigeerd voor leeftijd, want overgewicht komt vaker voor op hogere leeftijd, wat weer een risicofactor op zich is. Ook dan hebben mensen met obesitas nog 5,5 keer zo vaak diabetes type 2 als mensen zonder overgewicht, drie keer zo vaak hypertensie en twee keer vaker artrose en hart- en vaatziekten.

 Bron: medisch contact Heleen Croonen

De cijfers van het CBS

 Online gepubliceerd op: 28 januari 2014

Schildklier

Geplaatst op door

Thyroid Supplements With a Kick

 

Advice on money and health.

Feeling sluggish? Having a hard time getting out of bed in the morning? Gaining weight?

Many people with vague symptoms like these turn to dietary supplements that promise to jump-start metabolism by bolstering their thyroids with a mix of vitamins and minerals. Bladderwrack seaweed, iodine and an herb called ashwagondha are among the common ingredients.

But these over-the-counter products may also contain something that’s not so natural: thyroid hormones that should only be dispensed by prescription.

Tony Cenicola/The New York Times

Researchers who tested 10 popular thyroid-boosting products sold online found that nine contained the hormones thyroxine (T4) or triiodothyronine (T3), sometimes both. The amounts varied, but in some cases the recommended daily dose contained amounts of thyroid hormone as high or higher than delivered by prescription medications, according to the report, published in November in Thyroid, a scientific journal.

At the recommended daily dose of four capsules, one supplement delivered 91 micrograms of T4 and 16.5 micrograms of T3, the researchers found. In clinical practice, the starting dose of T4 for patients with low thyroid function is just 25 micrograms a day; some older patients are given half that amount. A dose of 75 micrograms a day is sufficient to restore function in many petite women.

“This supplement could give you as much thyroid hormone as you get in a prescription drug or more,” said Dr. Victor Bernet, chairman of endocrinology at the Mayo Clinic in Jacksonville, Fla., and senior author of the study. He became interested in so-called thyroid-support supplements after seeing a patient with inexplicable test results. The patient eventually admitted that he had been taking a supplement that a friend recommended for “low energy.”

 

Thyroid disease is common — and more common in women, affecting one in 10 over age 50. Patients may suffer fatigue, lethargy and weight gain, but not everyone with those symptoms has the illness. Patients taking thyroid hormone should be checked regularly by a physician, Dr. Bernet said.

“Thyroid hormone has a narrow therapeutic window,” he said, and “it’s easy to go over or under” the optimal dosages.

Taking too much can disrupt the body’s ability to regulate hormone levels, and actually may trigger thyroid disease in a healthy person, Dr. Bernet said. Excessive doses of thyroid hormone also can cause anxiety, insomnia and emotional changes, as well as bone loss and serious heart problems.

Officials with trade groups that represent supplement manufacturers said they were troubled by the study’s findings and would welcome regulatory enforcement against what one called the “few bad actors” producing adulterated products.

“No dietary supplements should contain prescription drugs, period,” said John Shaw, chief executive officer of the Natural Products Association. “They are illegal and should be removed from the market,” he said, adding, “We don’t want dangerous products out there.”

Both Mr. Shaw and Duffy MacKay, of the Council for Responsible Nutrition, another supplement trade association, suggested the tested products did not represent all of them, even though nine of 10 contained detectable levels of medication.

Mr. MacKay, a naturopathic doctor, said most consumers do not use “obscure” products like thyroid-support supplements. “This is a real fringe category, the outsiders of the outsiders of the outsiders,” he said.

While the Food and Drug Administration can take action against unsafe supplements once they are on the market, the regulations governing supplements differ substantially from those for conventional medications, which go through extensive testing before approval. Under the Dietary Supplement Health and Education Act of 1994, supplement manufacturers are required to ensure that products are safe before putting them on the market.

An F.D.A. spokeswoman said the agency has stepped up enforcement in recent years, in one case issuing warning letters about widespread violations of good manufacturing practices at an Atrium Inc. plant in Wautoma, Wis., that makes red yeast rice and other supplements. She declined to say whether the agency would be investigating thyroid-support products.

Doctors are also concerned about iodine, an ingredient in about half the thyroid-boosting supplements. In order for the body to make thyroid hormone, it needs iodine, but excessive amounts of the element may be harmful, Dr. Bernet noted.

The recent study did not analyze the iodine content in thyroid-support supplements, but labels on five of the products listed it as an ingredient, with amounts of 100 to 240 micrograms in the recommended daily dose. The recommended daily allowance for adults is 150 micrograms (slightly more for women who are pregnant or breast-feeding). A teaspoon of iodized salt contains 400 micrograms.

For iodine, as for thyroid hormone, Dr. Bernet said, there is a “sweet spot” in the diet; too much or too little may be harmful.

He and his co-authors did not make it easy for consumers who want to avoid supplements contaminated with thyroid hormone: The published paper did not identify the tested products.

Dr. Bernet’s advice was to avoid all of these supplements. “You can’t trust any of these things. You don’t know what’s in them.”

More on nytimes.com

Darmflora

Geplaatst op door

Probiotica is door de World Health Organization gedefinieerd als “levende kleine organismen die een positieve uitwerking hebben op de gezondheid van de mens wanneer deze in grote hoeveelheden worden ingenomen”. Probiotica zijn dus zogenaamde “goede bacteriën” en de bacteriën die worden gebruikt in probiotica zijn meestal gelijk aan de bacteriën die normaal gehuisvest zijn in de darmen. Deze goede bacteriën doen wat extra’s voor het lichaam en dragen bij aan een goede darmflora. De term darmflora wordt gebruikt om de miljarden bacteriën aan te duiden die in de darmen leven. Een goede darmflora is onder andere belangrijk voor de spijsvertering welke wordt ondersteund door alle bacteriën die in de darmen zitten. Een evenwichtige darmflora is eveneens belangrijk voor een goed werkend immuunsysteem en goede stoelgang.

Prébiotica

Prébiotica (inuline en fructo-oligosacchariden (FOS)) zijn onverteerbare voedingsvezels en zorgen er onder andere voor dat lactobacillen en bifidobacteriën (de goede bacteriën) beter kunnen groeien. Bovenal is uit onderzoek gebleken dat een prebiotica gecombineerd met een probiotica effectiever in het darmkanaal werkt dan de één of ander apart ingenomen.

Ontwikkeling van de darmflora

Tijdens de bevalling wordt de basis voor de darmflora al gelegd. De baby komt voor het eerst met bacteriën in aanraking door contact met het geboortekanaal, de moeder en de omgeving direct na de geboorte. De darmflora wordt voor het grootste deel samengesteld de periode direct na de geboorte. Een kind dat op de reguliere manier ter wereld komt heeft daardoor een andere darmflora samenstelling dan een kind dat via een keizersnede wordt geboren. Na ongeveer 30 dagen is de darmflora van een kind dat middels een keizersnede ter wereld wordt gebracht pas gelijk aan die van een kind die via de reguliere route ter wereld is gekomen. De bacteriën passeren de maag, omdat een baby nog niet veel maagzuur produceert, en vestigen zich op de darmwand. Kolonisatie van de bacteriën kan geschieden doordat er in eerste instantie bacteriën in de darmen aanwezig zijn die al het zuurstof gebruiken. Dit baant een weg voor de bacteriën die kunnen overleven zonder zuurstof (lactobacillen, bifidobacteriën). Vanaf dat moment kunnen deze in aantal toenemen en kan de darmflora zich ontwikkelen met allerlei bacteriën die voor ieder individu anders zijn.

Variatie darmflora

Iedere darmflora is uniek en vergelijkbaar met een vingerafdruk. Doordat de samenstelling zo uniek is, is het lastig te definiëren wat een normale darmflora is. Onderzoek heeft uitgewezen dat ieder individu dezelfde darmflora-kern heeft. Echter beslaat deze kern maar 20% van alle bacteriën die aanwezig zijn in de darmen. De overige 80% is bij een ieder verschillend. Er wordt gesuggereerd dat er maar liefst 1500 verschillende bacteriën aanwezig zijn. Op dit moment wordt daar nog uitvoerig onderzoek naar gedaan.

Bacteriële dysbiose

Om gezond te blijven is het belangrijk de darmflora in balans te houden. Door enkele factoren kan de darmflora echter uit balans raken. Hierbij moet gedacht worden aan het gebruik van antibiotica. Antibiotica staat er om bekend schadelijke bacteriën te doden, maar daarnaast doden ze ook de goede bacteriën in ons maag-darmkanaal. Leeftijd en voeding kunnen eveneens een rol spelen bij de verstoring van de harmonie in de darmen. Bij ouderen bestaat nog maar 1% van de totale darmflora uit bifidobacteriën waar dit bij volwassenen 3-6% is.

Probiotica is belangrijk bij het bestrijden van allerlei verschillende spijsverteringsproblemen. Een goede darmflora is namelijk onmisbaar bij het verteren van ons voedsel. Onze darmflora en enzymen zijn volledig verantwoordelijk voor het verteren van voedsel en opname van voedingsstoffen uit dit voedsel. Wanneer er een bacteriële dysbiose ontstaat en dit systeem niet meer naar behoren functioneert blijven er onnodige hoeveelheden etensresten achter in de darmen, die vervolgens tot ontstekingen kunnen leiden. Hiermee kan probiotica preventief werken en een effectief wapen zijn tegen het ontstaan van ontstekingen en het ontstaan van een verhoogde permeabiliteit van de darmwand met alle gevolgen van dien.

Stammen Probiotica

Het is belangrijk dat de bacteriën in de Probiotica levend aankomen op de eindbestemming, de darmen. Daarom is het belangrijk dat ze zuur-en gal resistent zijn. Hier is uitvoerig onderzoek naar verricht. In tabel 1 is te zien dat vrijwel alle bacteriën zuur-en gal resistent blijken te zijn met Lactobacillus Acidophilus als echte uitblinker op dit gebied.

Schermafbeelding 2014-01-20 om 15.27.59

Tabel 1: In vitro % herstel levende cellen na incubatie in medium met 1 van de factoren

Probiotica hebben de kracht om bepaalde ziekteverwekkers te remmen. Ook in onze stammen is dit nader bekeken bij bepaalde bekende ziekteverwekkers. Uit de resultaten komt naar voren dat vrijwel alle stammen de mogelijkheid hebben de verschillende onderzochte ziekteverwekkers maximaal te remmen. Hoe hoger het cijfer, hoe hoger de remming van die bepaalde ziekteverwekker (figuur 1 & tabel 2).

Figuur 1: De ziekteverwekkers werden gekweekt in een petrischaaltje met Agar-Agar (groeimedium die gebruikt wordt om micro organismen in te kweken). De probiotische stam werd aangebracht in het kleine holletje. In de Controle situatie is er geen remming van de ziekteverwekker (0). In het voorbeeld van goede remming wordt een maximale remming gemeten (3)
Schermafbeelding 2014-01-20 om 15.29.54
Figuur 1: De ziekteverwekkers werden gekweekt in een petrischaaltje met Agar-Agar (groeimedium die gebruikt wordt om micro organismen in te kweken). De probiotische stam werd aangebracht in het kleine holletje. In de Controle situatie is er geen remming van de ziekteverwekker (0). In het voorbeeld van goede remming wordt een maximale remming gemeten (3)

 

 

 

 

Schermafbeelding 2014-01-20 om 15.29.41

 

 

 

 

 

 

 

 

 

Tabel 2: 0= geen remming van de ziekteverwekker, 1= 8-11 mm, 2 = 11-14 mm 3= >14 mm maximale remming van de ziekteverwekker

T-cel differentiatie

Probiotica kunnen het immuunsysteem activeren door signalen vanuit het lumen via dendritische cellen aan het systeem door te geven. Het immuunsysteem wordt gereguleerd door twee hoofdcategorieën cytokines met verschillende functies en geproduceerd door subsets van T-helper (Th) lymfocyten.

Th1-cellen produceren voornamelijk IL-2 en interferon-γ en reguleren de immuunrespons tegen intracellulaire infecties. Th2-cellen produceren voornamelijk IL-4, IL-5 en IL-13 en zijn juist mediatoren in extracellulaire infecties en atopische ziektes. Regulatorische T-cellen (Treg) zijn de belangrijkste spelers die ervoor kunnen zorgen dat de balans van Th1/Th2 cellen terug naar homeostase gaan. Zoals in de onderstaande afbeelding wordt getoond, activeren de dendritische cellen bepaalde naïeve T-cellen (zijn nog niet in aanraking geweest met een antigeen) die zich vervolgens ontwikkelen tot een van deze meer specifieke T-cellen, die uiteindelijk de bijbehorende cytokines uitscheiden en een immuun reactie uitlokken (figuur 2).
Schermafbeelding 2014-01-20 om 15.31.39

Figuur 2: Dentrische cellen activeren bepaalde naïeve cellen T-cellen

Onze stammen zijn getest op hun mogelijkheid om het afweersysteem positief te beïnvloeden. Alle stammen laten zien dit te doen. Iedere stam had de mogelijkheid naïeve T-cellen te laten prolifereren in een specifieke T-cel. Dit was bevestigd door het meten van cytokine productie.
Bron: beyondmedicine

5 home remedies for ageing skin

Geplaatst op door

Have you ever imagined snails crawling across your face or leeches feasting on your blood? If you think this is some form of torture, wake up to the world of extreme beauty treatment. In the search for ageless skin, people all over the world are looking for exotic beauty treatments that promise a youthful glow. But don’t worry if you’re not in favour of such disconcerting therapies; your kitchen holds several goodies that can help you keep ageing skin at bay.

Schermafbeelding 2014-01-20 om 10.22.19Lemon juice to reduce age spots

The vitamin C present in lemons is a strong antioxidant. Besides, its bleaching action works wonders on age spots and freckles. Just squeeze out the juice from a lemon, apply and leave on your skin for about 15 minutes every day and then rinse with plain water.

For even better results, combine 1 teaspoon of lemon juice with half teaspoon of milk cream and 1 teaspoon of egg white. Mix all these ingredients and apply on the face; after 15 minutes, rinse with cold water.

Lemon juice in combination with honey is also a very effective remedy for ageing skin because honey has a soothing action. Mix one teaspoon each of lemon juice and honey and massage it into your skin. Keep for 20 minutes and then wash with warm water. (Read: When life gives you lemons, you slather them on your face!)

Coconut milk to moisturise dry skin

Coconut is a treasure-trove of vitamins and minerals; it also has the ability to moisturise your skin and keep it soft, supple and radiantly young. Grate raw coconut and squeeze the milk out of it. Apply this coconut milk onto your face; stay for about 20 minutes and then rinse it out with warm water. (Read: Tips to manage dry skin)

Papaya mask for skin firmness

You may know about papaya being good for the eyes because it has a lot of vitamin A; the same reason ensures it has a strong antioxidant action and this makes it good for your skin, too. Besides, the enzyme called papain in papaya can digest the dead cells on the surface of the skin and makes skin more elastic and firm. To make a papaya mask, cut a few pieces of a totally ripe papaya fruit and mash into a smooth paste. Apply this on the face and after 15 minutes, wash away with warm water.

Rose water to tighten skin

Rose water is a cleanser and can help remove the dirt clogging the pores of the skin. It also has an astringent action which means it tightens the skin; this helps it to give firmness and reduce the puffiness under the eyes. Mix 2 teaspoons of rose water with 3-4 drops of glycerine and half a teaspoon of lemon juice. Apply this mixture to your face using cotton ball every night before you go to bed.

Or you can also make a face pack by mixing in a teaspoon of rose water into a mixture of 1 teaspoon each of curd and honey. Add this mixture into a mashed ripe banana; apply the pack to your face and after 20 minutes, wash it with cool water.

Cucumber and curd pack to rejuvenate skin and under-eye skin

Cucumber helps to reduce the puffiness and dark circles under the eyes; besides it also has a soothing action that keeps skin healthy. Curd contains lactic acid which has the property of exfoliating the dead cells of the skin and this helps to rejuvenate the skin. Prepare a face mask by mixing half-cup curd with two teaspoons of grated cucumber and apply this to the skin. After 20 minutes, rinse with warm water. Using this face pack about twice a week for a few months will help keep your skin healthy and young.

While the local application of a face pack can help prevent ageing, it is equally important to strengthen the skin from within by providing it the right nutrition. Vegetables, fruits, fish oils and nuts such as almond and walnut are valuable sources of antioxidants, vitamins, minerals and omega-3 fatty acids and help to keep your skin young and healthy. So make sure you eat a healthy, balanced diet and use the right nutrients on your skin and you don’t ever need to worry about leeches and snails on your skin.

Vit E reduceert botbreuken

Geplaatst op door

 
Intake and serum concentrations of α-tocopherol in relation to fractures in elderly women and men: 2 cohort studies1,2,3
 

  1. Karl Michaëlsson,
  2. Alicja Wolk,
  3. Liisa Byberg,
  4. Johan Ärnlöv, and
  5. Håkan Melhus

+Author Affiliations


  1. 1From the Department of Surgical Sciences, Orthopedics, Uppsala University, Uppsala, Sweden (KM and LB); the Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (AW); the School of Health and Social Studies, Dalarna University, Falun, Sweden (JÄ); the Department of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden (JÄ); and the Department of Medical Sciences, Clinical Pharmacology, Uppsala University, Uppsala, Sweden (HM).

+Author Notes

  • ↵2 Supported by the Swedish Research Council, grant numbers 2008-2202 and 2009-6281. This is a free access article, distributed under terms (http://www.nutrition.org/publications/guidelines-and-policies/license/) that permit unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

  • ↵3 Address correspondence and reprint requests to K Michaëlsson, Department of Surgical Sciences, Section of Orthopedics, Uppsala University SE-751 85 Uppsala, Sweden. E-mail: karl.michaelsson@surgsci.uu.se.

 

Abstract

Background: A reduction in the formation of free radicals and oxidative stress might reduce the rate of bone loss and muscle wasting.

Objective: The objective was to determine whether α-tocopherol intake or serum concentrations are associated with fracture risk in older women and men.

Design: Two cohort studies, the Swedish Mammography Cohort (SMC; n = 61,433 women) and the Uppsala Longitudinal Study of Adult Men (ULSAM; n = 1138 men), were used.

Results: During 19 y of follow-up, 14,738 women in the SMC experienced a first fracture at any site (3871 hip fractures). A higher hip fracture rate was observed with lower intakes of α-tocopherol. Compared with the highest quintile of intake, the lowest quintile had a multivariable-adjusted HR of 1.86 (95% CI: 1.67, 2.06). The HR of any fracture was 1.20 (95% CI: 1.14, 1.28). α-Tocopherol–containing supplement use was associated with a reduced rate of hip fracture (HR: 0.78; 95% CI: 0.65, 0.93) and any fracture (HR: 0.86; 95% CI: 0.78, 0.94). Compared with the highest quintile of α-tocopherol intake in ULSAM (follow-up: 12 y), lower intakes (quintiles 1–4) were associated with a higher rate of hip fracture (HR: 3.33; 95% CI: 1.43, 7.76) and any fracture (HR: 1.84; 95% CI: 1.18, 2.88). The HR for hip fracture in men for each 1-SD decrease in serum α-tocopherol was 1.58 (95% CI: 1.13, 2.22) and for any fracture was 1.23 (95% CI: 1.02, 1.48).

Conclusion: Low intakes and low serum concentrations of α-tocopherol are associated with an increased rate of fracture in elderly women and men.

 

INTRODUCTION

Osteoporotic fractures constitute a large and growing problem worldwide in both women and men, with a profound effect on quality of life (1) and mortality (2). Fracture risk is influenced by both genetic constitution and by environmental factors, and lifestyle factors (eg, diet and physical activity) become of greater importance with increasing age (3).

During the past decade, it has become evident that the increase in oxidative stress with aging is a fundamental pathogenetic mechanism of age-related bone loss (4) and also possibly sarcopenia (5, 6)—2 important determinants that contribute to the risk of fracture (7–9). Research suggests a progressive decrease in both bone and muscle mass by 1–2%/y after the age of 50 y (5).

A reduction in the formation of free radicals and oxidative stress might reduce the rate of bone loss and muscle wasting in the elderly (4, 5). Because α-tocopherol, the vitamin E component with the highest antioxidant activity, is a potent scavenger of free radicals, it has been postulated that this form of vitamin E may favorably influence bone and muscle mass because of its antioxidant properties (4, 5, 10, 11).

However, human studies on the effect of α-tocopherol in relation to bone health are few. Importantly, there are no longitudinal data concerning the most relevant clinical endpoint of osteoporosis, fractures. We therefore examined the relation between α-tocopherol intake and fracture rate in elderly women within the Swedish Mammography Cohort (SMC)4 (12) and validated the findings in the Uppsala Longitudinal Study of Adult Men (ULSAM) (13, 14)—2 community-based, longitudinal, and well-characterized cohorts.

 

SUBJECTS AND METHODS

Briefly, the SMC study started in 1987. All 90,303 women residing in 2 Swedish counties (Uppsala and Västmanland), born between 1914 and 1948, received a mailed invitation to a routine mammography screening. Enclosed with this invitation was a questionnaire covering diet (food-frequency questionnaire; FFQ) and lifestyle, which was completed by 74% of the women (12). In 1997, a subsequent expanded questionnaire was sent to those who were still living in the study area (response rate: 70%). The study sample with exclusions was described previously (12). In the current fracture study, 61,433 women with baseline data and 38,984 with data from 1997 were available for analysis. The studies were approved by the regional ethics committees at Karolinska Institutet, Stockholm, Sweden, and Uppsala University, Uppsala, Sweden, and all participants gave their informed consent.

Intakes of α-tocopherol and of other nutrients were estimated by multiplying the frequency of consumption of each food item by the nutrient content of age-specific portion sizes. The intakes were adjusted for total energy intake by using the residual method (15). α-Tocopherol intake estimated by the FFQ correlated with estimates from 14 repeated 24-h dietary-recall interviews evenly distributed over 1 y (r = 0.57) (16). Current use of vitamin E–containing supplements was reported in the second questionnaire.

The ULSAM cohort (13, 14) consists of 2322 men who were 50 y of age at enrollment in 1970–1974. The current analyses are based on the third examination cycle of the ULSAM cohort, when participants were ∼71 y of age (1991–1995). In all, 1138 men recorded their dietary intake during 7 consecutive days at the time of the third examination. Dietary habits were determined with an optically readable form of a 7-d dietary record that was based on a validated and previously used precoded menu book (17). The participants were given oral instructions by a dietitian on how to perform the dietary registration, and the amounts consumed were reported in household measurements or specified as portion sizes. The daily intake of α-tocopherol, energy, and other selected nutrients was calculated by using a database from the Swedish National Food Administration, which contains ∼1500 food items, drinks, and recipes. Serum α-tocopherol, adjusted for serum lipid concentrations (total serum cholesterol and triacylglycerols) (18), had been determined in a subgroup of 654 men, of whom 635 men had serum α-tocopherol also analyzed from samples collected at 50 y of age. HPLC was used for the analyses (19).

Fracture ascertainment

Fracture events in both cohorts were collated through linkage with the Swedish National Patient Registry and local outpatient registers within each county. The fracture collection in SMC began in 1987 and in ULSAM in 1991, and end of follow-up was 31 December 2010. Complete linkage with the register is rendered by the personal identity number provided to all Swedish residents. Any fracture event was defined as a hospital admission or an outpatient visit with an International Classification of Diseases 10th edition, diagnosis code of S12 through S92. Hip fracture cases were defined by codes S720 through S722. Incident fracture admissions were separated from readmissions (20), and only the first fracture event was used in the analysis.

Statistics

We estimated multivariable-adjusted HRs for risk of fracture by Cox proportional hazards regression in both cohorts. To minimize potential bias, the directed acyclic graph approach (21) was used to identify a suitable multivariable model. The multivariable models (adjusted for age, BMI, height, total energy and calcium intakes (all continuous), calcium and vitamin D supplementation (both dichotomous), educational level (≤9, 10–12, >12 y, or other), physical activity level [5 categories in SMC (12) and 4 in ULSAM (22)], smoking status (never, former, or current), estrogen replacement therapy (never, former, or current), and Charlson’s comorbidity index (continuous) were similar in all analyses in both cohorts, although we additionally considered serum 25-hydroxyvitamin D and serum retinol concentrations (determined by HPLC, atmospheric pressure chemical ionization and mass spectrometry (APCI-MS), HPLC-APCI-MS, at Vitas, Oslo, Norway; http://www.vitas.no) at age 71 y, cognitive function, and FRAX scores (the WHO fracture prediction algorithm) (23) in ULSAM (23, 24). Other potential covariates (such as retinol, vitamin C, SFAs, MUFAs, PUFAs, alcohol, and protein intakes) in the multivariable models only marginally changed the relations and were therefore not included in the models. To better account for changes in the diet during follow-up and to better represent long-term dietary intake in the SMC, intakes of α-tocopherol and other nutrients estimated from the FFQs were treated as cumulative average intakes and the covariates as time-dependent variables (12). Covariates not assessed in the baseline FFQ of the SMC (eg, smoking habits and physical activity) were imputed by the Markov chain Monte Carlo multiple imputation method. Nonlinear trends of fracture risk were analyzed by quintiles of the exposure and by using a restricted cubic spline Cox regression model. We used 4 knots placed at percentiles 5, 35, 65, and 95. Finally, given that low vitamin E intake might be related to mortality, we both compared cumulative incidence curves with Kaplan-Meier failure curves (25) and estimated subhazard ratios of fracture according to the method of Fine and Gray (26) to address the potential competing risk problem from mortality. Even though these methods are not considered appropriate for etiologic analysis (27), which is the purpose of our analysis, competing risk analysis can provide additional valuable information for risk prediction (27).

Both low bone mineral density (BMD) and low muscle mass can be regarded as 2 component causes of fractures. In a supplementary mechanistic analysis, we therefore aimed to study the association between α-tocopherol intake and these components. Osteoporosis at the total hip, the femoral neck, or the spine diagnosed by dual-energy X-ray absorptiometry (DXA; Lunar Prodigy) was determined in a subcohort of SMC (SMC-Clinical; n = 5022) (12). Lean muscle mass was also determined by DXA, and skeletal muscle index (SMI) was calculated as the appendicular lean muscle mass (legs and arms) divided by height2(kg/m2). Moreover, sarcopenia was defined as an SMI <5.45 (28). One to 3 months before the DXA scan, the participants responded to a third FFQ that included both dietary assessment and covariate information. The associations between α-tocopherol intake with BMD, lean muscle mass, osteoporosis, and sarcopenia were evaluated with linear and logistic regression. For these analyses, we used multivariable models as described above but additionally included serum 25-hydroxyvitamin D and retinol concentrations (determined by HPLC–atmospheric pressure chemical ionization–tandem mass spectrometry at Vitas, Oslo, Norway) as well as total fat mass assessed by DXA.

A flowchart describing SMC, SMC-Clinical, and ULSAM is displayed elsewhere (see Supplemental Figure 1 under “Supplemental data” in the online issue). Statistical analyses were performed by using Stata 11.2 (Stata Corp) and SAS version 9.3 (SAS Institute).

 

RESULTS

Fracture risk in women

Characteristics of the women in the SMC at baseline (1987–1990) are displayed in Table 1. With increasing energy-adjusted dietary α-tocopherol intake, only modest differences were observed in reported intakes of energy, calcium, and vitamin D. In addition, only small differences were noted in the number of comorbidities, educational level, physical activity, and smoking status between quintiles of dietary α-tocopherol intake.

TABLE 1

Some baseline characteristics of the women in the Swedish Mammography Cohort by quintiles of energy-adjusted dietary α-tocopherol intake

During an average of 19 y of follow-up, 14,738 women experienced any type of first fracture (3871 of these were hip fractures). The multivariable-adjusted HRs for the risk of hip fracture (panel A) and any type of fracture (panel B) in the SMC in relation to energy-adjusted dietary intake of α-tocopherol are given in Figure 1. An exponential increase in hip fracture rate was discerned at intakes less than ∼5 mg/d, although the fracture rate was successively lowered also above this level without reaching a clear threshold. Compared with the highest quintile intake (median: 6.8 mg/d, Table 2), the lowest quintile intake (median: 4.3 mg/d) conferred a multivariable-adjusted HR of 1.86 (95% CI: 1.67, 2.06). The corresponding HR of any fracture was 1.20 (95% CI: 1.14, 1.28).

FIGURE 1.

Multivariable-adjusted restricted cubic spline Cox’s regression curve with 4 kn for the relation between dietary intake of α-tocopherol (the distribution is displayed by the rag plot above the x axis) and time to a first hip fracture (A) and any type of fracture (B) in women within the Swedish Mammography Cohort. The HR is indicated by the solid line and the 95% CI by the dashed lines. The reference was set at 8 mg/d, which is the recommended α-tocopherol intake for Swedish women. The HRs were adjusted for age, BMI, height, total energy intake, total calcium intake (all continuous), calcium (yes or no) and vitamin D (yes or no) supplementation, educational level (low, medium, high, or other), physical activity level (5 categories), smoking status (never, former, or current), and Charlson’s comorbidity index (continuous).

TABLE 2

HRs for hip fracture and for any type of fracture derived from Cox proportional hazards models in relation to quintiles of dietary α-tocopherol intake in the Swedish Mammography Cohort1

Moreover, current vitamin E–containing supplement use was reported by 10,801 of 38,984 women (28%) at the second questionnaire survey and was thereafter associated with a reduced rate of hip fracture (multivariable-adjusted HR: 0.78; 95% CI: 0.65, 0.93) and any type of fracture (HR: 0.86; 95% CI: 0.78, 0.94). The proportion of vitamin E supplement users was 30% in the highest baseline quintile of dietary α-tocopherol intake and 26% in the lowest quintile.

Fracture risk in men

Characteristics of the men in the ULSAM cohort at the third examination, by quintiles of α-tocopherol intake, are summarized in Table 3. Education, leisure physical activity, and energy, calcium, and vitamin D intakes tended to be higher in men with the highest quintile intake of α-tocopherol compared with lower intakes, whereas only small differences were seen in BMI and serum 25-hydroxyvitamin D concentrations. In addition, only 4% of the men reported use of any type of supplement. During an average follow-up of 12 y, 94 men had a hip fracture and 241 had any type of fracture. Low dietary intake was associated with a higher future fracture rate in men, but the association between dietary intake, α-tocopherol, and fracture rate was nonlinear (Table 4). Specifically, there was a tendency of higher rates of fracture observed in all of the first 4 quintiles compared with the highest quintile, although the estimates were not statistically significant for HRs of hip fracture in the 2 lowest quintiles. The lowest quintile intake of α-tocopherol, compared with the highest quintile, eg, was associated with a multivariable-adjusted HR for hip fracture of 2.23 (95% CI: 0.66, 7.54). The same comparison for any fracture conferred a statistically significant HR of 2.67 (95% CI: 1.33, 5.38). In comparison with the highest quintile intake (median: 8.1 mg/d), lower intake levels (quintiles 1–4) showed a multivariable-adjusted HR for hip fracture of 3.33; 95% CI: 1.43, 7.76) and an HR for any fracture of 1.84 (95% CI: 1.18, 2.88; data not shown in Table 4).

TABLE 3

Some baseline characteristics of the men in the Uppsala Longitudinal Study of Adult Men at age 71 y by quintiles of dietary α-tocopherol intake

TABLE 4

HRs for hip fracture and for any type of fracture derived from Cox proportional hazards models in relation to quintiles of dietary α-tocopherol intake in the Uppsala Longitudinal Study of Adult Men1

Characteristics of the men in ULSAM with serum α-tocopherol measurements (n = 654) are displayed inTable 5. During follow-up from age 71 y, we identified 51 men with an incident hip fracture and 139 with any type of fracture. Higher serum α-tocopherol was associated with a lower fracture rate, and the relation seemed to be linear for hip fracture (P = 0.59 for serum α-tocopherol as a quadratic term) and for any fracture (P = 0.70). A 1-SD (0.30 mg/mmol) decrease in serum α-tocopherol concentration at age 71 y was associated with a multivariable-adjusted HR of 1.58 (95% CI: 1.13, 2.22) for hip fracture and of 1.23 (95% CI: 1.02, 1.48) for any fracture. Moreover, for each 1-SD reduction (0.34 mg/mmol) in serum α-tocopherol between ages 50 and 71 y, the HR of hip fracture was 1.71 (95% CI: 1.15, 2.53) and of any fracture was 1.27 (95% CI: 1.02, 1.58). These associations are also displayed as spline curves elsewhere (see Supplemental Figure 2 under “Supplemental data” in the online issue).

TABLE 5

Some baseline characteristics of adult men at age 71 y with serum α-tocopherol measurements in the Uppsala Longitudinal Study

Mean (±SD) serum α-tocopherol concentrations in the highest quintile of dietary intake of α-tocopherol averaged 1.66 ± 0.29 mg/mmol compared with 1.60 ± 0.29 mg/mmol at lower intakes (P = 0.04). Only 28 men (2.5%) in the dietary survey reported use of vitamin E–containing supplements. They also had, on average, 0.18-mg/mmol (95% CI: 0.06, 0.30) higher serum α-tocopherol concentrations (P = 0.007) than did nonusers of vitamin E–containing supplements.

Competing risk

The cumulative incidence curves indicated that our results would not be compromised by competing risk from mortality (see Supplemental Figure 3 under “Supplemental data” in the online issue) in SMC and ULSAM (see Supplemental Figure 4 under “Supplemental data” in the online issue). Although we observed an excess mortality among women with a low α-tocopherol intake (see Supplemental Table 1a under “Supplemental data” in the online issue), the subhazard ratios of hip fracture were still elevated in these women (see Supplemental Table 1b under “Supplemental data” in the online issue).

α-Tocopherol intake, bone, and muscle

Characteristics of the subcohort SMC-Clinical are displayed elsewhere (see Supplemental Table 2 under “Supplemental data” in the online issue). Of these 5022 women with a mean age of 68 y, 1012 women had osteoporosis and 538 women were defined to have sarcopenia.

The intake of α-tocopherol intake was positively and independently associated with BMD and lean body mass. Thus, for each 3-mg decrease in α-tocopherol intake, the BMD of the proximal femur, after multivariable adjustment, decreased by 1.1% (95% CI: 0.3, 1.8; P = 0.005), the lumbar spine (L1-L4) by 0.8% (95% CI: −0.1, 1.8; P = 0.09), appendicular lean mass by 0.8% (95% CI: 0.2, 1.4; P = 0.01), and SMI by 0.6% (95% CI: 0.05, 1.18; P = 0.03). In addition, for every 3-mg decrease in α-tocopherol intake, the multivariable adjusted OR of osteoporosis at the lumbar spine was 1.20 (95% CI: 1.03, 1.41) and at the proximal femur was 1.46 (95% CI: 1.19, 1.78), and the OR of sarcopenia was 1.28 (95% CI: 1.04, 1.57). All Pvalues of a quadratic term of α-tocopherol intake in the models were >0.05, which indicated linear associations.

 

DISCUSSION

In 2 independent cohorts we observed a higher rate of fracture in the elderly that was associated with low intakes of α-tocopherol. There was also a higher risk of both osteoporosis and sarcopenia with low intakes of α-tocopherol. Furthermore, the validity of these findings was corroborated by the relation between low serum α-tocopherol concentrations and a higher rate of fracture in men.

No previous prospective studies have assessed the relation between intakes or serum concentrations of α-tocopherol with future fracture risk. In previous cross-sectional studies, hip fracture patients had low vitamin E concentrations compared with control subjects at the time of the fracture event (29), and higher postoperative vitamin E concentrations were associated with lower concentrations of inflammatory markers (30). High serum concentrations of vitamin E were related to better physical function after the hip fracture (31). In animal models, supplementation with α-tocopherol improved fracture healing (10, 32–34). Interestingly, no association was found between BMD and vitamin E intake or serum vitamin E concentrations in the Women’s Health Initiative Observational Study and Clinical Trial (35). However, it must be emphasized that the participants had a total vitamin E intake averaging 29 mg/d (35), ie, substantially higher than that of the participants in the current investigation (mean: 5 mg/d). It must also be underscored that the rates of fracture in our studies were similar at intakes >10 mg/d, ie, no apparent further decrease in fracture rate was noted above this amount. Moreover, our group previously presented data indicating a negative influence of high oxidative stress and a beneficial effect of high vitamin E concentrations on bone within our Scandinavian setting (36–38).

Possible explanations and implications

Vitamin E has been proposed to have positive effects on both bone and muscle mass owing to its antioxidant properties (4–6, 10, 11), rendering a theoretical consequential lower fracture risk with a higher α-tocopherol intake. Our results support these experimental findings: higher intakes were associated with higher BMD, higher lean muscle mass, and lower fracture risk. In addition, recent randomized trials have indicated that vitamin E and C supplements have a positive effect on BMD and muscle mass in elderly women and men (39–41). Nevertheless, our results at first seem to contrast with experimental findings by Fujita et al (42), who recently found that a high intake of α-tocopherol was deleterious for bone health. However, the researchers fed 4-wk-old mice and rats a diet supplemented with 600 mg α-tocopherol/kg, which corresponds to a supplement that is almost 30 times higher than the amount recommended in rodents (43). Accumulating high doses of α-tocopherol given to young rodents could be toxic (44) and lead to loss of appetite, reduced weight gain, and depressed bone growth. High dietary levels of vitamin E may also negatively affect the utilization of vitamin D3 and lead to reduced bone mass (45). In addition, as shown in a meta-analysis of randomized studies, although low to moderate doses of vitamin E supplements might modestly reduce all-cause mortality (46), very high doses of vitamin E supplements (average dose: 400 mg/d) (46) may increase mortality in humans and is therefore not recommended (46). On the other hand, a corresponding dose given to rodents had anabolic bone effects (10). The highest percentile dietary α-tocopherol intakes in the SMC were 10 and 13 mg/d in ULSAM. We were therefore not able to consider the association between high-dose intakes of α-tocopherol and fracture risk.

The consumption of α-tocopherol is low in Sweden and other Scandinavian countries (47). Only ∼10% of the women in the SMC and 5% of the men in ULSAM had an intake higher than the Swedish recommended intakes (8 and 10 mg/d for women and men, respectively). The highest incidences of osteoporotic fractures worldwide are also found in Scandinavia (48)—an observation that cannot readily be explained by known lifestyle or genetic determinants, climate, or longevity.

Strengths and weaknesses of the study

The strengths of the SMC were the size of the cohort, the population-based design, the large number of fractures, and the repeated FFQs. Because of the individual personal identification number of all Swedish residents, in combination with nationwide health care registers, we were able to identify almost all fractures that occurred in the cohort. However, we recognize that our study had limitations that should be considered when interpreting the results. First, one limitation common to observational studies is that they preclude conclusions regarding causality. Whether an interventional increased intake of α-tocopherol corresponds to a lower risk of fractures remains to be established. Importantly, findings from observational studies indicating that increases in vitamin E intake might reduce cardiovascular disease, diabetes mellitus, and cancer have not been confirmed in randomized trials with very high intakes of α-tocopherol (49–51). We did have the possibility to adjust our estimates for comorbidities, lifestyle factors, other nutrients, and a low vitamin D status (serum 25-hydroxyvitamin D concentrations), which is a frailty indicator in both men (52) and women (53), but the possibility of residual confounding still remains. In particular, people who use dietary supplements have, on average, a healthier lifestyle and a lower risk factor profile for cardiovascular disease (54), which could additionally lower their fracture risk (55). We considered the potential competing risk problem from mortality by the method of Fine and Gray (26) and by cumulative incidence curves (25). The subhazard ratios were similar to the HRs from the ordinary Cox regression, which suggests no major effect of competing risk, although it must also be emphasized that subhazard ratios are not directly comparable with ordinary cause-specific HRs (56). The latter estimates are the preferred measure of association in etiologic analysis (27)—the major focus of our study. Dietary-assessment methods are subject to many limitations that affect both the precision and accuracy of the measurement. An FFQ is used to assess the habitual intake of diet in larger studies such as the SMC, and a recent review concluded that it is a valid method for assessing dietary vitamin E intake (57). Nevertheless, the dietary recording in ULSAM can be regarded as a more precise dietary method with less misclassification (57), which, in combination with the homogeneous age in this cohort, may explain the somewhat stronger association with fracture rate in ULSAM compared with the SMC. However, we cannot exclude that these differences may reflect sex differences in the underlying pathology of osteoporotic fractures. By using the ULSAM cohort, although with a lower number of fractures rendering less precise estimates, we were able to replicate the findings from the SMC, which was a further strength of our study. Moreover, we were able to establish an association between serum concentrations of α-tocopherol and future fracture risk.

In conclusion, our observational data indicate that vitamin E insufficiency is associated with higher fracture risk. Additional studies are warranted to confirm our novel discoveries and ultimately randomized clinical trials that evaluate the effect on fracture risk of low doses (daily recommended intake) of vitamin E.

 

Acknowledgments

The authors’ responsibilities were as follows—KM: designed the study, drafted the manuscript, and had primary responsibility for the final content; KM and LB: analyzed the data; and LB, HM, JÄ, and AW: contributed to the interpretation of the data and revision of the manuscript. All authors read and approved the final manuscript. None of the authors declared a conflict of interest.

 

Footnotes

  • ↵4 Abbreviations used: APCI-MS, atmospheric pressure chemical ionization and mass spectrometry; BMD, bone mineral density; DXA, dual-energy X-ray absorptiometry; FFQ, food-frequency questionnaire; SMC, Swedish Mammography Cohort; SMI, skeletal muscle index; ULSAM, Uppsala Longitudinal Study of Adult Men.

 

  • Received April 17, 2013.
  • Accepted October 25, 2013.

 

This is a free access article, distributed under terms (http://www.nutrition.org/publications/guidelines-and-policies/license/) that permit unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

 

REFERENCES

  1. 1.↵
    1. Riggs BL,
    2. Melton Iii LJ

    . The worldwide problem of osteoporosis: insights afforded by epidemiology. Bone 1995;17:505S–11S.

  2. 2.↵
    1. Center JR,
    2. Nguyen TV,
    3. Schneider D,
    4. Sambrook PN,
    5. Eisman JA

    . Mortality after all major types of osteoporotic fracture in men and women: an observational study. Lancet 1999;353:878–82.

  3. 3.↵
    1. Michaëlsson K,
    2. Melhus H,
    3. Ferm H,
    4. Ahlbom A,
    5. Pedersen NL

    . Genetic liability to fractures in the elderly. Arch Intern Med 2005;165:1825–30.

  4. 4.↵
    1. Manolagas SC,
    2. Parfitt AM

    . What old means to bone. Trends Endocrinol Metab 2010;21:369–74.

  5. 5.↵
    1. Cerullo F,
    2. Gambassi G,
    3. Cesari M.

    . Rationale for antioxidant supplementation in sarcopenia. J Aging Res 2012;2012:316943.

  6. 6.↵
    1. Meng SJ,
    2. Yu LJ

    . Oxidative stress, molecular inflammation and sarcopenia. Int J Mol Sci2010;11:1509–26.

  7. 7.↵
    1. Marshall D,
    2. Johnell O,
    3. Wedel H

    . Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures. BMJ 1996;312:1254–9.

  8. 8.
    1. Järvinen TL,
    2. Sievanen H,
    3. Khan KM,
    4. Heinonen A,
    5. Kannus P

    . Shifting the focus in fracture prevention from osteoporosis to falls. BMJ 2008;336:124–6.

  9. 9.↵
    1. Fiatarone Singh MA,
    2. Singh NA,
    3. Hansen RD,
    4. Finnegan TP,
    5. Allen BJ,
    6. Diamond TH,
    7. Diwan AD,
    8. Lloyd BD,
    9. Williamson DA,
    10. Smith EU,
    11. et al

    . Methodology and baseline characteristics for the Sarcopenia and Hip Fracture study: a 5-year prospective study. J Gerontol A Biol Sci Med Sci 2009;64:568–74.

  10. 10.↵
    1. Shuid AN,
    2. Mohamad S,
    3. Muhammad N,
    4. Fadzilah FM,
    5. Mokhtar SA,
    6. Mohamed N,
    7. Soelaiman IN

    . Effects of alpha-tocopherol on the early phase of osteoporotic fracture healing. J Orthop Res 2011;29:1732–8.

  11. 11.↵
    1. Mehat MZ,
    2. Shuid AN,
    3. Mohamed N,
    4. Muhammad N,
    5. Soelaiman IN

    . Beneficial effects of vitamin E isomer supplementation on static and dynamic bone histomorphometry parameters in normal male rats. J Bone Miner Metab 2010;28:503–9.

  12. 12.↵
    1. Warensjö E,
    2. Byberg L,
    3. Melhus H,
    4. Gedeborg R,
    5. Mallmin H,
    6. Wolk A,
    7. Michaelsson K

    . Dietary calcium intake and risk of fracture and osteoporosis: prospective longitudinal cohort study. BMJ 2011;342:d1473.

  13. 13.↵
    1. Michaëlsson K,
    2. Lithell H,
    3. Vessby B,
    4. Melhus H

    . Serum retinol levels and the risk of fracture. N Engl J Med 2003;348:287–94.

  14. 14.↵
    1. Michaëlsson K,
    2. Baron JA,
    3. Snellman G,
    4. Gedeborg R,
    5. Byberg L,
    6. Sundstrom J,
    7. Berglund L,
    8. Arnlov J,
    9. Hellman P,
    10. Blomhoff R,
    11. et al

    . Plasma vitamin D and mortality in older men: a community-based prospective cohort study. Am J Clin Nutr 92:841–8.

  15. 15.↵
    1. Willett WC,
    2. Howe GR,
    3. Kushi LH

    . Adjustment for total energy intake in epidemiologic studies. Am J Clin Nutr 1997;65(suppl 4):1220S–8S.

  16. 16.↵
    1. Messerer M,
    2. Johansson SE,
    3. Wolk A

    . The validity of questionnaire-based micronutrient intake estimates is increased by including dietary supplement use in Swedish men. J Nutr 2004;134:1800–5.

  17. 17.↵
    1. Nydahl M,
    2. Gustafsson IB,
    3. Mohsen R,
    4. Becker W

    . Comparison between optical readable and open-ended weighed food records. Food Nutr Res (Epub ahead of print 20 February 2009).

  18. 18.↵
    1. Thurnham DI,
    2. Davies JA,
    3. Crump BJ,
    4. Situnayake RD,
    5. Davis M

    . The use of different lipids to express serum tocopherol: lipid ratios for the measurement of vitamin E status. Ann Clin Biochem1986;23:514–20.

  19. 19.↵
    1. Arnlöv J,
    2. Zethelius B,
    3. Riserus U,
    4. Basu S,
    5. Berne C,
    6. Vessby B,
    7. Alfthan G,
    8. Helmersson J

    . Uppsala Longitudinal Study of Adult Men. Serum and dietary beta-carotene and alpha-tocopherol and incidence of type 2 diabetes mellitus in a community-based study of Swedish men: report from the Uppsala Longitudinal Study of Adult Men (ULSAM) study. Diabetologia 2009;52:97–105.

  20. 20.↵
    1. Gedeborg R,
    2. Engquist H,
    3. Berglund L,
    4. Michaelsson K

    . Identification of incident injuries in hospital discharge registers. Epidemiology 2008;19:860–7.

  21. 21.↵
    1. Shrier I,
    2. Platt RW

    . Reducing bias through directed acyclic graphs. BMC Med Res Methodol2008;8:70.

  22. 22.↵
    1. Michaëlsson K,
    2. Olofsson H,
    3. Jensevik K,
    4. Larsson S,
    5. Mallmin H,
    6. Berglund L,
    7. Vessby B,
    8. Melhus H

    .Leisure physical activity and the risk of fracture in men. PLoS Med 2007;4:e199.

  23. 23.↵
    1. Byberg L,
    2. Gedeborg R,
    3. Cars T,
    4. Sundstrom J,
    5. Berglund L,
    6. Kilander L,
    7. Melhus H,
    8. Michaelsson K

    .Prediction of fracture risk in men: a cohort study. J Bone Miner Res 2012;27:797–807.

  24. 24.↵
    1. Melhus H,
    2. Snellman G,
    3. Gedeborg R,
    4. Byberg L,
    5. Berglund L,
    6. Mallmin H,
    7. Hellman P,
    8. Blomhoff R,
    9. Hagstrom E,
    10. Arnlov J,
    11. et al

    . Plasma 25-hydroxyvitamin D levels and fracture risk in a community-based cohort of elderly men in Sweden. J Clin Endocrinol Metab 2010;95:2637–45.

  25. 25.↵
    1. Lin DY

    . Non-parametric inference for cumulative incidence functions in competing risks studies.Stat Med 1997;16:901–10.

  26. 26.↵
    1. Fine J,
    2. Gray R

    . A proportional hazards model for the subdistribution of a competing risk. J Am Stat Assoc 1999;94:496–509.

  27. 27.↵
    1. Lau B,
    2. Cole SR,
    3. Gange SJ

    . Competing risk regression models for epidemiologic data. Am J Epidemiol2009;170:244–56.

  28. 28.↵
    1. Baumgartner RN,
    2. Koehler KM,
    3. Gallagher D,
    4. Romero L,
    5. Heymsfield SB,
    6. Ross RR,
    7. Garry PJ,
    8. Lindeman RD

    . Epidemiology of sarcopenia among the elderly in New Mexico. Am J Epidemiol1998;147:755–63.

  29. 29.↵
    1. D’Adamo CR,
    2. Shardell MD,
    3. Hicks GE,
    4. Orwig DL,
    5. Hochberg MC,
    6. Semba RD,
    7. Yu-Yahiro JA,
    8. Ferrucci L,
    9. Magaziner JS,
    10. Miller RR

    . Serum vitamin E concentrations among highly functioning hip fracture patients are higher than in nonfracture controls. Nutr Res 2011;31:205–14.

  30. 30.↵
    1. D’Adamo CR,
    2. Miller RR,
    3. Shardell MD,
    4. Orwig DL,
    5. Hochberg MC,
    6. Ferrucci L,
    7. Semba RD,
    8. Yu-Yahiro JA,
    9. Magaziner J,
    10. Hicks GE

    . Higher serum concentrations of dietary antioxidants are associated with lower levels of inflammatory biomarkers during the year after hip fracture. Clin Nutr 2012;31:659–65.

  31. 31.↵
    1. D’Adamo CR,
    2. Miller RR,
    3. Hicks GE,
    4. Orwig DL,
    5. Hochberg MC,
    6. Semba RD,
    7. Yu-Yahiro JA,
    8. Ferrucci L,
    9. Magaziner J,
    10. Shardell MD

    . Serum vitamin E concentrations and recovery of physical function during the year after hip fracture. J Gerontol A Biol Sci Med Sci 2011;66:784–93.

  32. 32.↵
    1. Durak K,
    2. Sonmez G,
    3. Sarisozen B,
    4. Ozkan S,
    5. Kaya M,
    6. Ozturk C

    . Histological assessment of the effect of alpha-tocopherol on fracture healing in rabbits. J Int Med Res 2003;31:26–30.

  33. 33.
    1. Turk C,
    2. Halici M,
    3. Guney A,
    4. Akgun H,
    5. Sahin V,
    6. Muhtaroglu S

    . Promotion of fracture healing by vitamin E in rats. J Int Med Res 2004;32:507–12.

  34. 34.↵
    1. Kurklu M,
    2. Yildiz C,
    3. Kose O,
    4. Yurttas Y,
    5. Karacalioglu O,
    6. Serdar M,
    7. Deveci S

    . Effect of alpha-tocopherol on bone formation during distraction osteogenesis: a rabbit model. J Orthop Traumatol2011;12:153–8.

  35. 35.↵
    1. Wolf RL,
    2. Cauley JA,
    3. Pettinger M,
    4. Jackson R,
    5. Lacroix A,
    6. Leboff MS,
    7. Lewis CE,
    8. Nevitt MC,
    9. Simon JA,
    10. Stone KL,
    11. et al

    . Lack of a relation between vitamin and mineral antioxidants and bone mineral density: results from the Women’s Health Initiative. Am J Clin Nutr 2005;82:581-8.

  36. 36.↵
    1. Melhus H,
    2. Michaelsson K,
    3. Holmberg L,
    4. Wolk A,
    5. Ljunghall S

    . Smoking, antioxidant vitamins, and the risk of hip fracture. J Bone Miner Res 1999;14:129–35.

  37. 37.
    1. Basu S,
    2. Michaelsson K,
    3. Olofsson H,
    4. Johansson S,
    5. Melhus H

    . Association between oxidative stress and bone mineral density. Biochem Biophys Res Commun 2001;288:275–9.

  38. 38.↵
    1. Ostman B,
    2. Michaelsson K,
    3. Helmersson J,
    4. Byberg L,
    5. Gedeborg R,
    6. Melhus H,
    7. Basu S

    . Oxidative stress and bone mineral density in elderly men: antioxidant activity of alpha-tocopherol. Free Radic Biol Med2009;47:668–73.

  39. 39.↵
    1. Ruiz-Ramos M,
    2. Vargas LA,
    3. Fortoul Van der Goes TI,
    4. Cervantes-Sandoval A,
    5. Mendoza-Nunez VM

    .Supplementation of ascorbic acid and alpha-tocopherol is useful to preventing bone loss linked to oxidative stress in elderly. J Nutr Health Aging 2010;14:467–72.

  40. 40.
    1. Chuin A,
    2. Labonte M,
    3. Tessier D,
    4. Khalil A,
    5. Bobeuf F,
    6. Doyon CY,
    7. Rieth N,
    8. Dionne IJ

    . Effect of antioxidants combined to resistance training on BMD in elderly women: a pilot study. Osteoporos Int 2009;20:1253–8.

  41. 41.↵
    1. Labonté M,
    2. Dionne IJ,
    3. Bouchard DR,
    4. Senechal M,
    5. Tessier D,
    6. Khalil A,
    7. Labonte M,
    8. Bobeuf F,
    9. Tessier D,
    10. Khalil A,
    11. et al

    . Effects of antioxidant supplements combined with resistance exercise on gains in fat-free mass in healthy elderly subjects: a pilot study. J Am Geriatr Soc 2008;56:1766–8.

  42. 42.↵
    1. Fujita K,
    2. Iwasaki M,
    3. Ochi H,
    4. Fukuda T,
    5. Ma C,
    6. Miyamoto T,
    7. Takitani K,
    8. Negishi-Koga T,
    9. Sunamura S,
    10. Kodama T,
    11. et al

    . Vitamin E decreases bone mass by stimulating osteoclast fusion. Nat Med2012;18:589–94.

  43. 43.↵
    National Research Council, Subcommittee on Laboratory Animal Nutrition. Nutrient requirements of laboratory animals. 4th rev. ed. Washington, DC: National Academy of Sciences, 1995.
  44. 44.↵
    1. Yasunaga T,
    2. Kato H,
    3. Ohgaki K,
    4. Inamoto T,
    5. Hikasa Y

    . Effect of vitamin E as an immunopotentiation agent for mice at optimal dosage and its toxicity at high dosage. J Nutr 1982;112:1075–84.

  45. 45.↵
    1. Aburto A,
    2. Britton WM

    . Effects of different levels of vitamins A and E on the utilization of cholecalciferol by broiler chickens. Poult Sci 1998;77:570–7.

  46. 46.↵
    1. Miller ER 3rd.,
    2. Pastor-Barriuso R,
    3. Dalal D,
    4. Riemersma RA,
    5. Appel LJ,
    6. Guallar E

    . Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2005;142:37–46.

  47. 47.↵
    1. Jenab M,
    2. Salvini S,
    3. van Gils CH,
    4. Brustad M,
    5. Shakya-Shrestha S,
    6. Buijsse B,
    7. Verhagen H,
    8. Touvier M,
    9. Biessy C,
    10. Wallstrom P,
    11. et al

    . Dietary intakes of retinol, beta-carotene, vitamin D and vitamin E in the European Prospective Investigation into Cancer and Nutrition cohort. Eur J Clin Nutr 2009;63(suppl 4):S150–78..

  48. 48.↵
    1. Kanis JA,
    2. Oden A,
    3. McCloskey EV,
    4. Johansson H,
    5. Wahl DA,
    6. Cooper C

    , on behalf of the IOFWGoE.Quality of L. A systematic review of hip fracture incidence and probability of fracture worldwide.Osteoporos Int 2012;23:2239–56.

  49. 49.↵
    1. Lee IM,
    2. Cook NR,
    3. Gaziano JM,
    4. Gordon D,
    5. Ridker PM,
    6. Manson JE,
    7. Hennekens CH,
    8. Buring JE

    . Vitamin E in the primary prevention of cardiovascular disease and cancer: the Women’s Health Study: a randomized controlled trial. JAMA 2005;294:56–65.

  50. 50.
    1. Song Y,
    2. Cook NR,
    3. Albert CM,
    4. Van Denburgh M,
    5. Manson JE

    . Effects of vitamins C and E and beta-carotene on the risk of type 2 diabetes in women at high risk of cardiovascular disease: a randomized controlled trial. Am J Clin Nutr 2009;90:429–37.

  51. 51.↵
    1. Lin J,
    2. Cook NR,
    3. Albert C,
    4. Zaharris E,
    5. Gaziano JM,
    6. Van Denburgh M,
    7. Buring JE,
    8. Manson JE

    . Vitamins C and E and beta carotene supplementation and cancer risk: a randomized controlled trial. J Natl Cancer Inst 2009;101:14–23.

  52. 52.↵
    1. Ensrud KE,
    2. Blackwell TL,
    3. Cauley JA,
    4. Cummings SR,
    5. Barrett-Connor E,
    6. Dam TT,
    7. Hoffman AR,
    8. Shikany JM,
    9. Lane NE,
    10. Stefanick ML,
    11. et al

    . Circulating 25-hydroxyvitamin D levels and frailty in older men: the osteoporotic fractures in men study. J Am Geriatr Soc 2011;59:101–6.

  53. 53.↵
    1. Ensrud KE,
    2. Ewing SK,
    3. Fredman L,
    4. Hochberg MC,
    5. Cauley JA,
    6. Hillier TA,
    7. Cummings SR,
    8. Yaffe K,
    9. Cawthon PM

    . Study of osteoporotic fractures research g. circulating 25-hydroxyvitamin D levels and frailty status in older women. J Clin Endocrinol Metab 2010;95:5266–73.

  54. 54.↵
    1. Rautiainen S,
    2. Akesson A,
    3. Levitan EB,
    4. Morgenstern R,
    5. Mittleman MA,
    6. Wolk A

    . Multivitamin use and the risk of myocardial infarction: a population-based cohort of Swedish women. Am J Clin Nutr2010;92:1251–6.

  55. 55.↵
    1. Sennerby U,
    2. Melhus H,
    3. Gedeborg R,
    4. Byberg L,
    5. Garmo H,
    6. Ahlbom A,
    7. Pedersen NL,
    8. Michaelsson K

    .Cardiovascular diseases and risk of hip fracture. JAMA 2009;302:1666–73.

  56. 56.↵
    1. Andersen PK,
    2. Geskus RB,
    3. de Witte T,
    4. Putter H

    . Competing risks in epidemiology: possibilities and pitfalls. Int J Epidemiol 2012;41:861–70.

  57. 57.↵
    1. Henríquez-Sánchez P,
    2. Sanchez-Villegas A,
    3. Doreste-Alonso J,
    4. Ortiz-Andrellucchi A,
    5. Pfrimer K,
    6. Serra-Majem L

    . Dietary assessment methods for micronutrient intake: a systematic review on vitamins.Br J Nutr 2009;102(suppl 1):S10–37.

 

Vreemde lichaamskwaaltjes die op vitaminetekort wijzen

Geplaatst op door

 

 Foxnews.com
© Thinkstock.

Je lichaam kan je op vreemde manieren iets proberen te vertellen, bijvoorbeeld dat je een tekort hebt aan cruciale vitamines. Professor Susan Blum legt uit dat door een grote consumptie verwerkte voeding je makkelijk met vitaminetekorten kunt kampen.

Een vitaminetekort wijst ofwel op een tekort van de juiste voedingstoffen of dat je lichaam deze stoffen niet kan opnemen. Je gaat hier niet ziek van worden, maar hierdoor functioneert je lichaam wel niet naar behoren, omdat vitamines vaak betrokken zijn bij heel wat biochemische reacties in het lichaam. Het goede nieuws is dat je de meeste van deze problemen met kleine aanpassingen aan het voedingspatroon kunt oplossen. Als dit niet lukt, breng je best een bezoekje aan de dokter. 

Scheurtjes aan de mond 
Tekort: IJzer, zink en vitamine B. Dit probleem treft vaak vegetariërs. Het komt ook voor wanneer je te weinig proteïne opneemt door een strikt dieet. 

Oplossing: Geniet wat vaker van kip, zalm, tonijn, eieren, oesters, mosselen, zongedroogde tomaten, pindanoten en linzen. De absorptie van ijzer wordt versterkt door vitamine C, deze stof helpt ook infecties te bestrijden, combineer deze voeding daarom met groenten als broccoli, rode paprika en bloemkool. 

Rode uitslag en haarverlies
Tekort: Biotine, ook bekend als B7. Je lichaam kan dit namelijk niet opslaan. 

Oplossing: Eet meer gekookte eieren, zalm, avocado, chamignon, bloemkool, sojabonen, noten, frambozen en bananen. 

Witte en rode bultjes op de wangen, armen, dijen en achterwerk
Tekort: Essentiële vetzuren, vitamine A en D. 

Oplossing: Schrap verzadigde en transvetten en verhoog de opname van gezonde vetten. Dit doe je door meer zalm, sardines, amandelen, walnoten en lijnzaad te eten. Je neemt meer vitamine A op met groene bladgroenten en kleurrijke groenten als wortelen, zoete aardappelen en rode paprika’s. Dit zijn goede bronnen van betacaroteen, deze stof heeft je lichaam nodig om vitamine A aan te maken. De opname van vitamine D ligt moeilijker, want zonlicht stimuleert de productie hiervan in je lichaam, tijdens de wintermaanden neem je dus best een voedingssupplement.  

Tintelende of gevoelloze handen en voeten 
Tekort: Vitamines B als foliumzuur, B6 en B12. Dit is een tekort dat onmiddellijk effect heeft op de zenuwen die eindigen in de huid, vandaar het vreemde gevoel in de ledematen. Deze symptomen kunnen gepaard gaan met angsten, depressies, bloedtekort, vermoeidheid en een verstoord hormonaal evenwicht. 

Oplossing: Eet meer spinazie, asperges, bieten, bonen, eieren, inktvis, mosselen, oesters en gevogelte. 

Spierkrampen in de tenen, kuiten en voeten 
Tekort: Magnesium, calcium en kalium. Als je regelmatig krampen krijgt in je onderlichaam, kan dit wijzen op een tekort van deze stof. Wie erg hard traint, kan meer mineralen verliezen door hevige transpiratie. 

Oplossing: Zet meer bananen, amandelen, hazelnoten, pompoenen, kersen, appels, pompelmoes, broccoli en donkergroene bloedgroenten als boerenkool en spinazie op het menu.

Blijf op de hoogte; vul uw emailadres in of voeg me toe als vriend