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Kronisk Inflammasjon Kosthold og livsstil som slukker brannen

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Presentasjon om: "Kronisk Inflammasjon Kosthold og livsstil som slukker brannen"— Utskrift av presentasjonen:

1 Kronisk Inflammasjon Kosthold og livsstil som slukker brannen
Fedon Alexander Lindberg Spes.i indremedisin-Dr. Lindbergs Klinikk

2 Livsstilsykdommer: Verdens største helseproblem
Hjerte- og karsykdom (nr.1 årsak til prematur død) Kreft (nr.2 årsak til prematur død) Metabolsk Syndrom Overvekt -diabetes type 2 Muskel-, skjelett- og Leddlidelser Psykiske plager

3 Vi tygger piller som aldri før
Medikamentforbruket har økt fra 6,6 mrd i 1990 til godt over 18,6 mrd i 2011 (i 2002-kroner) Kr.1559 Kr. 3790 Medisinbruk pr. innbygger

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5 Kolesterolsenkende midler i Norge På midten av 1990-tallet kom det første kolesterol- eller lipidsenkende midlene på markedet. Siden har flere midler kommet til, og salget har økt voldsomt. Figuren viser salget av lipidsenkende midler, oppgitt i form av såkalt definerte døgndoser (DDD) per 1000 innbyggere per døgn.

6 Blodtrykksmedisiner - forbruk i Norge Salget av blodtrykksmedisiner økte for alvor fra slutten av 1980-tallet. Det viser den øverste kurven i samlefiguren nedenfor.

7 Polymåltid vs Polypille
The Polypill. A strategy to reduce cardiovascular disease by more than 80%. Wald NJ, Law MR. BMJ Jun 28;326(7404):1419. The Polymeal: a more natural, safer, and probably tastier (than the Polypill) strategy to reduce cardiovascular disease by more than 75%. Franco OH, Bonneux L, de Laet C, Peeters A, Steyerberg EW, Mackenbach JP. BMJ Dec 18;329(7480):

8 The Polymeal 1 glass of wine daily (150cc)
400gram (~1lb) assorted fruits and vegetables daily 110gram (~4oz) fish 4 times a week 60gram (~2oz) of almonds daily 100gram (~3oz) dark chocolate daily 2,8 gram (1 clove) of garlic daily

9 Hippokrates of Kos Medisinens Far 460-370 f.Kr.
”…Du er hva du spiser… …La Mat være din Medisin…” ”…Det som er bra for hjertet er bra for hjernen…”

10 Nåtidens kosthold – mye feil mat
Altfor mye junk food (bearbeidede produkter) Altfor mye raske karbohydrater Poteter, fint hvetemel, finere brød Altfor mye sukker Altfor mye salt Altfor mye feil fett (billige planteoljer og margariner) For mye transfett (herdet vegetabilsk fett) i f.eks. kjeks, brød, wienerbrød …og altfor lite grønnsaker, fisk

11 Hvilket kosthold er vi programmert til?
Menneskets evolusjon… Genene våre har gjennomgått en 7 mill år lang evolusjonsutvikling Historisk sett er vi programmert til lite, men naturlig mat og mye slit Når det gjelder utviklingen av menneskets gener, snakker vi om kanskje så mye som 7 mill år med evolusjonshistorie. Homo sapiens er ca år gammel. Faktisk har våre gener forandret seg med 0,1% de siste årene. Fram til midten av det forrige århundret har menneskets hverdag for det meste bestått av lite mat og mye slit. Denne hverdagen er det våre gener er best ”utrustet” til.

12 Våre gener er i steinalderen – 98% av dem er identisk med sjipansens
Steinalderen Sanking Jakt Sesongtilgang Landbruksrevolusjonen Korn Husdyr Kjøtt & melk Mindre fysisk aktivitet Industrirevolusjonen Poteter Sukker Raffinert hvetemel Enda mindre fysisk aktivitet McDonaldisering Lettvint / tilgjengelig Bearbeidede produkter Maskiner / bil Kontorarbeide

13 Hva styrer vårt kosthold
Lettvinthet Tilgjengelighet Pris Media Smak Næringsverdi

14 Hvilken livsstil er vi programmert til?
Menneskets evolusjon… Genene våre har gjennomgått en 7 mill år lang evolusjonsutvikling Historisk sett er vi programmert til lite, men naturlig mat og mye slit

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16 Hva er viktig for oss? Vi kan klare oss uten alt annet unntatt: MAT
VANN LUFT SOLLYS Disse elementers kvalitet er avgjørende for vår helse

17 1.2% skiller oss, men hvem er klokest?

18 Lavkarbo, Høykarbo eller Smartkarbo?
Hvilket kosthold kan sørge for bedre helse og lengre liv?

19 Kostholdsforvirret?? Da er du en av 73% nordmenn
Høykarbo eller lavkarbo? Sunt med masse brød og poteter eller egg og bacon hver morgen? Pøse på med fløte og smør eller «kolesterolsenkende-hjertevennlige» margariner? Hvem skal man tro og hvorfor?

20 Tre enkle prinsipper: 1. Velg oftest naturlig ubearbeidet mat
2. Mest mat fra planter 3. Helst ikke for mye om gangen

21 Inflammation, AGING AND CHRONIC DISEASE Chronic systemic inflammation is an underlying cause of many seemingly unrelated, age-related diseases. As humans grow older, systemic inflammation can inflict devastating degenerative effects throughout the body (Ward 1995; McCarty 1999; Brod 2000). Correcting a chronic inflammatory disorder will enable many of the health problems of aging to be prevented or reversed.

22 Inflammasjon:Fellesnevner bak de fleste kroniske sykdommer
Følgende mekanismer er involvert Oksidasjon Glykosylering Metylering Eikosanoidbalanse

23 The Causes of Age-Related Inflammation
Aging results in an increase of inflammatory cytokines that contribute to the progression of many degenerative diseases (Van der Meide et al. 1996; Licinio et al. 1999). Rheumatoid arthritis is a classic autoimmune disorder in which excess levels of cytokines such as TNF-a, IL-6, IL-1(b), and/or IL-8 are known to cause or contribute to the inflammatory syndrome (Deon et al. 2001). Chronic inflammation is also involved in diseases as diverse as atherosclerosis, cancer, heart valve dysfunction, obesity, diabetes, congestive heart failure, digestive system diseases, and Alzheimer's disease (Brouqui et al. 1994; Devaux et al. 1997; De Keyser et al. 1998).

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30 The Causes of Age-Related Inflammation (2)
In aged people with multiple degenerative diseases, the inflammatory marker, C-reactive protein, is often sharply elevated, indicating the presence of an underlying inflammatory disorder (Invitti 2002; Lee et al. 2002; Santoro et al. 2002; Sitzer et al. 2002). When a cytokine blood profile is conducted on people in a weakened condition, an excess level of one or more of the inflammatory cytokines, e.g., TNF-a, IL-6, IL-1(b), or IL-8, is usually found (Santoro et al. 2002).

31 The Causes of Age-Related Inflammation (2)
In aged people with multiple degenerative diseases, the inflammatory marker, C-reactive protein, is often sharply elevated, indicating the presence of an underlying inflammatory disorder (Invitti 2002; Lee et al. 2002; Santoro et al. 2002; Sitzer et al. 2002). When a cytokine blood profile is conducted on people in a weakened condition, an excess level of one or more of the inflammatory cytokines, e.g., TNF-a, IL-6, IL-1(b), or IL-8, is usually found (Santoro et al. 2002).

32 Elevated TNF-a in well treated hypertension
TNF-a levels were measured in a group of people with high blood pressure and a group with normal blood pressure (Verdecchia et al. 2002). The hypertensive subjects taking anti-hypertensive medications had about the same blood pressure as the healthy test subjects. Arterial flow medicated dilation, however, was significantly impaired in the hypertensives and this group also showed higher levels of TNF-a, indicating persistent inflammation despite blood pressure control. This study showed that even when blood pressure is under control, hypertensives still suffer endothelial dysfunction caused by a chronic inflammatory insult.

33 Elevated C-Reactive Protein and Interleukin-6 Predict Type II Diabetes
Baseline levels of C-reactive protein and interleukin-6 (IL-6) were significantly higher among those who subsequently developed diabetes compared to those who did not. (Pradhan et al. 2001). Women with the higher IL-6 levels were 7.5 times more likely to develop diabetes while those in the higher C-reactive protein ranges were 15.7 times more likely to become diabetic. After adjusting for all other known risk factors, women with the highest IL-6 levels were 2.3 times at greater risk, while those with the highest C-reactive protein levels were 4.2 times more likely to become diabetic. These other diabetic risk factors (such as obesity, estrogen replacement therapy and smoking) all sharply increase inflammatory markers in the blood. These data support a possible role for inflammation in diabetogenesis.

34 C-Reactive Protein and IL-6 Predict Death
Elevated C-reactive protein, IL-6 and other inflammatory cytokines indicate significantly greater risks of contracting or dying from specific diseases (heart attack, stroke, Alzheimer's disease, etc.). 1,293 healthy elderly people were followed for a period of 4.6 years (Harris et al. 1999). Higher IL-6 levels were associated with a twofold greater risk of death. Higher C-reactive protein was also associated with a greater risk of death, but to a lesser extent than elevated IL-6. Subjects with both high C-reactive protein and IL-6 were 2.6 times more likely to die during follow up than those with low levels of both of these inflammation markers. These results were independent of all other mortality risk factors.

35 Diet and chronic inflammation
Foods can potentially cause or reduce inflammation Some foods cause more inflammation than others Inflammation is mediated through chemical substances called cytokines, which all cells produce - eicosanoids/cytokines Eicosanoids are made of essential fatty acids (omega 3 and 6) Eicosanoid balance is affected by - hormones (among others insulin, cortisol) - type of fat we eat - several micro nutrients (vitamins-minerals)

36 Oxidation and inflammation affect all organs, not least the brain, because of its high fat content
Everything that contributes to less oxidation and inflammation will have a universall positive health effect

37 Oksidasjon og Inflammasjon
Oksidasjon står sentralt Oksygen er livsviktig men fører til gradvis oksidasjon i kroppen Prooksidanter: - mat, økt blodsukker, (flere)umettet fett, stress, røyking, miljøgifter, jern med mer Antioksidanter: Viktigst er vårt endogene antioksidantsystem (Glutathion, Liponsyre, Superoxid dismutase, Urinsyre, Melatonin) - vitaminer (for eksempel vit E, C, beta karoten), noen mineraler (for eksempel selen), fytokjemikalier (polyfenoler med mer), stressmestring, god og nok søvn, ren luft, unngå miljøgifter med mer). Antioxidant status kan testes i blodprøve

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39 Add colour to your diet for antioxidant protection

40 Foods with Antioxidant Power
Per 100grams Chocolate, cloves, allspice, cinnamon, saffron, coffee, oregano, sage, thyme Blueberries 2234 Blackberries 2036 Kale 1770 Strawberries 1536 Spinach, raw 1210 Raspberries 1227 Plums 949 Alfalfa sprouts 931 Spinach, steamed 909 Broccoli 888 Beetroot Avocado 782 Orange 750 Grape, red 739 Pepper, red 731 Cherry 670 Kiwifruit 602 Beans, baked 503 Grapefruit, pink 483 Beans, kidney 460 Onion 449 Corn 402 Peas, frozen 364 Potatoes, sweet 301 Cantaloupe 252 Apple 281 Carrots 207

41 Glycation's Role in Inflammation Cooking and Aging have similar Biological Properties
Glycation can be described as the binding of a protein molecule to a glucose molecule resulting in the formation of damaged protein structures- AGE or Advanced Glycation Endproducts. (Maillard-Amidori reaction). Many age-related diseases such as arterial stiffening, cataract and neurological impairment are at least partially attributable to glycation. AGE render proteins in the body cross-linked and barely functional. As AGE accumulate, they cause cells to emit signals that induce the production of inflammatory cytokines.

42 Glycation IN VIVO Glycation occurs in vivo when blood glucose reacts with body proteins. AGE production is much higher in diabetes Consuming low glycemic foods prevents excessive glycation. The higher the glycemic load (GL) of the diet, the more AGE are produced. The insulin surge that contributes to chronic inflammatory processes. It is also important to avoid over consumption of foods high in omega 6 arachidonic acid (beef, egg yolk, dairy, etc.).

43 Cooking, glycation and inflammation
Glycation occurs ex vivo during cooking in high temperatures (browning effect) and little or no water (frying, high temp.oven baking, grilling). Approximately 10-20% of AGE in food gets absorbed by the gut. AGE form in the skin, arteries, eye lenses, joints, cartilage, etc. Consuming foods high in AGE might be responsible for the induction of a low-grade, but chronic state of inflammation.

44 JUNK FOOD, glycation and inflammation
Since most "junk" foods are cooked at extremely high temperatures, it makes sense to avoid French fries, hamburgers, potato chips, fried food and other snacks. These foods not only contain lots of glycotoxins, they also create other metabolic disorders that can induce degenerative disease.

45 Methylation Chemical reactions that go on in every cell in your body by which methyl groups (one atom of carbon and three atoms of hydrogen) are transferred into another molecule. When this does not happen in a complete manner, intermediary molecules are created, which create free radicals and damage DNA. One of the best examples of this is the creation of homocysteine, which can damage arteries and cause heart disease. Cancer is another possible outcome of this process. To address this, you need to ensure that your diet contains precursors for methylated DNA. These are called methyl donors and can help ensure proper methylation reactions necessary for gene expression take place in your body.

46 Methylation, the Homocystein Connection and Inflammation
Homocysteine is a toxic byproduct of normal protein metabolism- Enough Vitamin B6, B12 and folate keep it low

47 Homocysteine predicts risk for..
Heart attacks, strokes and blood clots Pregnancy problems and birth defects Memory deficit and Alzheimer’s disease Depression (especially in women) Schizophrenia (especially in young men) School grades Possibly autism … and is easily reversible with optimum nutrition

48 Optimal ‘Homocysteine’ Score is below 7-9 (“normal” is up to 15) Around 8-10% of the population has a gene variation (MTHFR) causing excessive homocysteine and need supplementation

49 8 Ways to Lower Your ‘Homocysteine’ Score below 7-9
Eat enough animal protein (less meat, more fish and vegetable protein, eggs, dairy)- for B12 Eat your greens Have a clove of garlic a day Cut back on coffee and black tea Limit your alcohol Reduce your stress Stop smoking Consider supplementing homocysteine lowering nutrients daily (Vitamin B12, B6 and folate)

50 OMEGA FATS, EICOSANOIDS AND INFLAMMATION
Omega-3 fatty acids found in fish oil help to suppress the formation of undesirable prostaglandin E2 and promote synthesis of beneficial prostaglandin E3 (Kelley et al. 1985; Watanabe et al. 2000). Similar mechanism as NSAID/COX inhibitors. Gamma - linolenic acid (GLA) induces production of the anti-inflammatory prostaglandin E1 (Das et al. 1989; Fan et al. 1997). What you eat can significantly affect whether you have more of the beneficial prostaglandins (E1 and E3) as opposed to the pro-inflammatory prostaglandin E2. Reducing the consumption of foods that are high in omega-6 fatty acids and increasing the consumption of omega-3 rich foods, such as salmon and other fish, can be beneficial.

51 OMEGA FATS, EICOSANOIDS AND INFLAMMATION
Limiting foods that convert to arachidonic acid can help reduce inflammation. Arachidonic acid is a precursor to both prostaglandin E2 and the pro-inflammatory cytokine leukotriene B(4) (Brock et al. 1999). Another dietary factor that can lead to high levels of arachidonic acid is the overconsumption of high-glycemic index carbohydrates that cause excess production of insulin (Kreisberg et al. 1983).

52 Omega 3 from fish reduce inflammation
Omega 3 fatty acid DHA (fish oil) is well documented as to its ability to suppress TNF-a, IL-6, IL-1(b), and IL-8 (Jeyarajah et al. 1999; James et al. 2000; Watanabe et al. 2000; Yano et al. 2000). Fish oil suppresses these dangerous cytokines by up to 90% (James et al. 2000).

53 Fettsyrer og eikosanoider
For mye omega-6 og for lite omega-3 i dagens kosthold Mengde og type omega-3 og omega-6 har betydning for hvilke eikosanoider som dannes og hvilke mengder av eikosanoider som dannes

54 Proinflammatoriske eikosanoider fra omega 6
serie 2 * byggesten: arakidonsyre (kilde: eggeplommer, animalsk fett) * stimuleres av insulin (karbohydrater) * eksempler: -tromboksan A2 (økt blodlevring) -PGE2 (demper immunforsvaret) -leukotriener (allergifremkallende)

55 Antiinflammatoriske eikosanoider fra omega 6
Serie 1 * byggesten: omega 6 fettsyrer (kilde: panteoljer, nøtter) * stimuleres av glukagon (protein) * eksempler: -PGE1 antitrombotisk øker fettforbrenningen øker insulinfølsomheten antiinflammatorisk demper astma-allergier

56 Antiinflammatoriske eikosanoider fra omega 3
Serie 3 * byggesten: omega 3 fettsyrer (kilde: fet fisk, nøtter, linfrø) antitrombotisk forebygger hjerte- og karsykdom bidrar til økt muskelmasse styrker immunforsvaret betennelsesdempende

57 Fettsyrer (2) Prostaglandinsyntesen
Δ-6-desaturase (krever Mg, B6) Hemmes av infeksjon (?), transfettsyrer, mettet fett, kroniske virusinfeksjoner Økt aktivitet ved høyt insulin n-3-fettsyrer α-linolensyre (ALA) n-6-fettsyrer cis-linolsyre (LA) γ-linolensyre (GLA) Stearidensyre Δ-6-elongase (krever B3?, B6?, Mg?) Di-homo-γ-linolensyre Eicosatraensyre Δ-5-desaturase økt aktivitet ved høyt insulin eller fettsyremangel hemmer Eicosapentaensyre (EPA) hemmer Clupanodensyre Cyclooxygenase Aktiviteten økes av alkohol (?) Aktiviteten hemmes av NSAIDs, Li, steroider, hvitløk, ingefær, EPA, vitamin c Arakidonsyre (AA) Docosahexa- Ensyre (DHA) Lipoxygenase Hemmes av E, DGLA, løk mm Leukotriener PGH1 PGH3 Kun ratebegrensende enzymer som er med? Les mer om syntesen. Få en oversikt over hva som styrer syntesen fra en annen kilde. Hvorfor fører ikke GLA til økning i AA? Finn fulltekst på artikler som beskriver regulering av desaturaser. Lipids Aug;24(8): Related Articles, Links Effect of magnesium deficiency on delta 6 desaturase activity and fatty acid composition of rat liver microsomes. Mahfouz MM, Kummerow FA. Burnsides Research Laboratory, University of Illinois, Urbana Experimental Mg2+ deficiency was induced in a group of rats by feeding them a Mg2+-deficient diet for 23 days. They were pair-fed to compare with a control group of rats fed a Mg2+-sufficient diet. In the Mg2+-deficient group the plasma total cholesterol and triglyceride levels were increased while HDL-cholesterol was decreased. In the Mg2+-deficient group the plasma level of thiobarbituric acid reacting substances (TBARS) used as a measure for lipid peroxidation was increased. The increase was attributed to the increased cytosolic Ca2+ in Mg2+-deficiency which can cause: 1) increase of hydro and endoperoxide levels as a consequence of the increase of arachidonic acid release and eicosanoid synthesis in Mg2+-deficiency, and 2) inhibition of the mitochondrial respiratory activity and activation of Ca2+-dependent proteases which may activate the conversion of xanthine dehydrogenase to xanthine oxidase which generates active O2 species. In the Mg2+-deficient group, the fatty acid composition of the liver microsomes indicated a slower rate of conversion of linoleic acid to arachidonic acid which was consistent with the decrease of delta 6 desaturase activity in liver microsomes of Mg2+-deficient rats as measured in vitro. The decrease of delta 6 desaturase activity was attributed to the lower concentration of actual enzyme molecules as a result of the decreased rate of protein synthesis in Mg2+-deficiency. The possible effects of the increased catecholamine release in Mg2+-deficiency are discussed Nutr Jul;114(7): Related Articles, Links Influence of reduced food intake on polyunsaturated fatty acid metabolism in zinc-deficient rats. Kramer TR, Briske-Anderson M, Johnson SB, Holman RT. The influence of reduced food intake on metabolism of liver phospholipids (PL) in zinc-deficient (ZD) rats was measured. Wealing male Long-Evans rats were fed ad libitum zinc-deficient (2 micrograms Zn/g diet) and zinc-adequate (20 micrograms Zn/g diet) diets for 21 days. A pair-fed (PF) group was included. ZD and PF rats displayed significantly increased levels of linoleic (18:2 omega 6) and dihomo-gamma-linolenic acid (20:3 omega 6). Both ZD and PF rats displayed increased levels of gamma-linolenic acid (18:3 omega 6), but the increase was significant only in PF rats. ZD and PF rats displayed decreased levels of arachidonic acid (20:4 omega 6), but the decrease was significant only in PF rats. Both ZD and PF rats displayed significantly reduced levels of 22:5 omega 6. Both ZD and PF rats displayed increased products of delta 6 desaturation and decreased products of delta 5 and delta 4 desaturation. Significantly increased products of delta 9 desaturation were noted in both ZD and PF rats. ZD and PF rats displayed significant increases in C20 elongation products. ZD and PF rats displayed significantly decreased levels of omega 6 metabolites but not total omega 6 acids. ZD rats showed significantly increased levels of total omega 3 acids and omega 3 metabolites. ZD and PF rats showed significant increases in omega 9 acids but not significant changes in omega 9 metabolites. This study does not indicate that zinc affects the delta 6 desaturase in the metabolism of essential fatty acids. The aberrations previously attributed to zinc deficiency are probably due to the accompanying decreased food intake. Prostaglandins Leukot Essent Fatty Acids Jun;58(6): Related Articles, Links Dual influence of aging and vitamin B6 deficiency on delta-6-desaturation of essential fatty acids in rat liver microsomes. Bordoni A, Hrelia S, Lorenzini A, Bergami R, Cabrini L, Biagi PL, Tolomelli B. Dipartimento di Biochimica G. Moruzzi, Bologna, Italy. Delta-6-desaturase (D6D) activity is influenced by many nutritional and non-nutritional factors, among which one of the most important is aging. D6D activity could be susceptible to the dual influence of aging itself and of nutritional deficiencies, due to the reduced intake and/or absorption of essential nutrients. Particularly, vitamin B6 deficiency might be a crucial factor for D6D activity in aged people. Using 20 month old Sprague-Dawley rats fed a diet with a subnormal level of vitamin B6, we evaluated D6D activity for linoleic acid (LA) and alpha-linolenic acid (ALA) in liver microsomes, and the fatty acid composition of microsomal total lipids. We observed a diminished D6D activity for LA and also for ALA in vitamin B6-deficient animals, being approximately 63% and 81% respectively of the corresponding activity in control rats. As a consequence, significant modifications in the relative molar content of microsomal fatty acids were observed. The content of arachidonic and docosahexaenoic acid, the main products of the conversion of LA and ALA respectively, decreased, LA content increased and a decrease in the unsaturation index was observed in liver microsomes of B6-deficient rats. The foregoing results suggest that the impairment of D6D activity by vitamin B6 deficiency might be an important factor in decreasing the synthesis of n-6 and n-3 PUFAs. This may be particularly important in aging, where D6D activity is already impaired. J Nutr Aug;133(8): Related Articles, Links   Dietary trans fatty acids alter the compositions of microsomes and mitochondria and the activities of microsome delta6-fatty acid desaturase and glucose-6-phosphatase in livers of pregnant rats. Larque E, Garcia-Ruiz PA, Perez-Llamas F, Zamora S, Gil A. Department of Physiology, University of Murcia, Murcia, Spain. This study was designed to investigate the effects of three diets with different levels of trans fatty acids and the physiologic status on the physicochemical properties and enzymatic activities of liver microsomes and mitochondria. Three groups of 10 female weaning rats each were fed for 10 wk one of three diets differing in their trans fatty acid contents (Control, 0 mol/100 mol total fatty acids; high, 14.5 mol/100 mol; very high, 30 mol/100 mol). At the onset of adult life (10 wk of age), they were mated. Six rats in each group were killed at the end of gestation (Pregnant rat groups). The four remaining pregnant rats continued to receive their experimental diets until weaning of their litters. Six pups from the litters for each group (3 males and 3 females) were selected and fed the same experimental diet as the dams from wk 3 to 10 of age (2nd generation virgin groups) and then killed. Trans fatty acid levels in liver microsomes and mitochondria rose in parallel with the dietary trans fatty acid content, whereas saturated fatty acids dropped in both organelles with increasing trans fatty acids. Pregnant and 2nd generation adult rats fed trans isomers also had lower levels of cholesterol and a lower cholesterol/phosphorus ratio in their liver microsomes compared with controls. A significant interaction between diet and pregnancy was detected in the activities of delta6-desaturase and glucose-6-phosphatase in liver microsomes. Dietary trans fatty acids decreased the activities of both enzymes but only in pregnant rats. No differences in the fluorescence anisotropy of membranes or the enzymatic activities in liver mitochondria were observed. In conclusion, dietary trans fatty acids significantly lowered cholesterol and the cholesterol/phosphorus ratio in liver microsomes. This effect might contribute to low delta6-desaturase and glucose-6-phosphatase activities in liver microsomes of pregnant rats. J Lipid Res Feb;31(2):271-7.Related Articles, Links   Interactions of saturated, n-6 and n-3 polyunsaturated fatty acids to modulate arachidonic acid metabolism. Garg ML, Thomson AB, Clandinin MT. Nutrition and Metabolism Research Group, University of Alberta, Edmonton, Canada. Anti-thrombotic effects of omega-3 (n-3) fatty acids are believed to be due to their ability to reduce arachidonic acid levels. Therefore, weanling rats were fed n-3 acids in the form of linseed oil (18:3n-3) or fish oil (containing 20:5n-3 and 22:6n-3) in diets containing high levels of either saturated fatty acids (hydrogenated beef tallow) or high levels of linoleic acid (safflower oil) for 4 weeks. The effect of diet on the rate-limiting enzyme of arachidonic acid biosynthesis (delta 6-desaturase) and on the lipid composition of hepatic microsomal membrane was determined. Both linseed oil- or fish oil-containing diets inhibited conversion of linoleic acid to gamma-linolenic acid. Inhibition was greater with fish oil than with linseed oil, only when fed with saturated fat. delta 6-Desaturase activity was not affected when n-3 fatty acids were fed with high levels of n-6 fatty acids. Arachidonic acid content of serum lipids and hepatic microsomal phospholipids was lower when n-3 fatty acids were fed in combination with beef tallow but not when fed with safflower oil. Similarly, n-3 fatty acids (18:3n-3, 20:5n-3, 22:5n-3, and 22:6n-3) accumulated to a greater extent when n-3 fatty acids were fed with beef tallow than with safflower oil. These observations indicate that the efficacy of n-3 fatty acids in reducing arachidonic acid level is dependent on the linoleic acid to saturated fatty acid ratio of the diet consumed. Alcohol Aug;34(1):27-33.Related Articles, Links   Perspectives on alcohol consumption: liver polyunsaturated fatty acids and essential fatty acid metabolism. Pawlosky RJ, Salem N Jr. Division of Intramural Clinical and Biological Research, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5625 Fishers Lane, Room 3C-07, Rockville, MD 20852, USA. In this article, subjects diagnosed with alcoholic liver disease are shown to have lower concentrations of several polyunsaturated fatty acids (PUFAs), including 18:2n6, 18:3n6, 20:3n6, 18:3n3, 22:5n3, and 22:6n3, but not 20:4n6 and 22:4n6, nor 22:5n6, in the total lipid extracts of their livers compared with findings for specimens obtained from patients diagnosed with primary biliary cirrhosis and from control subjects. Findings of studies in animals have demonstrated that prolonged alcohol consumption reduces liver polyunsaturate content. However, the effect of ethanol on the elongation/desaturation of essential fatty acids is complex, as in vitro study results indicate that the direction of the effect of alcohol may be related to the dose of alcohol. Findings of studies in hepatocyte cell culture indicate that ethanol increased delta-5 and delta-6 desaturase activities throughout a broad concentration range. In contrast, lower liver desaturase activity has been reported in animals consuming high concentrations of alcohol (36%-40% energy) over a period of several months. Findings from in vivo isotope tracers studies in nonhuman primates and felines indicate that prolonged periods of moderate (mean consumption 2.6 g kg(-1) d(-1) and 1.2 g kg(-1) d(-1), respectively) alcohol consumption had no effect on the uptake of either linoleic (18:2n6) or alpha-linolenic (18:3n3) acids into the plasma and lead to an increased incorporation of these deuterated precursors into 20:4n6 and 22:6n3. Thus, this likely reflects a stimulated, rather than an inhibited, production of long-chain PUFAs. In numerous studies in various species, investigators have documented that alcohol consumption can increase the level of lipid peroxidation in tissues, and sustained periods of ethanol-induced peroxidation can deplete tissues of PUFAs. A hypothesis to rationalize the long-term effects of alcohol consumption on liver PUFA concentration that takes into consideration the effect of ethanol on essential fatty acid metabolism is presented. Int J Tissue React Jun;3(2):89-94.Related Articles, Links Auto-immunity and prostaglandins. Das UN. Several auto-immune diseases have been described in human beings. Though the exact aetiological agent(s) is not known, clinical or subclinical viral infections and certain drugs are known to induce them. Hyperactivity of B-cells, possibly due to the loss of normal regulatory control by T-cells may account for the increased synthesis of auto-antibodies in these diseases. Prostaglandins (PGs) are known to regulate immune response and fibrous tissue formation. Deficiency of PGE1 and/or thromboxane A2 (TxA2) and excess PGE2 seem to activate B-cells and suppress T-Cell function and enhance fibrosis. Viruses are known to block the enzyme delta-6-desaturase necessary for PGE1 synthesis and thus depress cell-mediated immune response. Drugs known to cause autoimmune disorders also seem to block PGE1 and/or TxA2 synthesis and enhance PGE2 formation which may lead to excess auto-antibody formation. Drugs like colchicine known to enhance TxA2 formation and the biological actions of PGE1 were found to be of benefit in Behcet's syndrome, vasculitis, amyloidosis, scleroderma and in controlling the auto-immune disease in adjuvant arthritis in rats, the renal disease in NZB/W mice and passively transferred vasculitis. Thus altered PG function may play a major role in auto-immunity. Publication Types: Review PMID: [PubMed - indexed for MEDLINE]  Display   Show  Write to the Help Desk NCBI | NLM | NIH Department of Health & Human Services Privacy Statement | Freedom of Information Act | Disclaimer Curr Med Chem May;11(9): Related Articles, Links Non-antioxidant activities of vitamin E. Zingg JM, Azzi A. Institute of Biochemistry and Molecular Biology, University of Bern, Buhlstrasse 28, 3012 Bern, Switzerland. Molecules in biological systems often can perform more than one function. In particular, many molecules have the ability to chemically scavenge free radicals and thus act in the test tube as antioxidant, but their main biological function is by acting as hormones, ligands for transcription factors, modulators of enzymatic activities or as structural components. In fact, oxidation of these molecules may impair their biological function, and cellular defense systems exist which protect these molecules from oxidation. Vitamin E is present in plants in 8 different forms with more or less equal antioxidant potential (alpha-, beta-, gamma-, delta-tocopherol/tocotrienols); nevertheless, in higher organisms only alpha-tocopherol is preferentially retained suggesting a specific mechanism for the uptake for this analogue. In the last 20 years, the route of tocopherol from the diet into the body has been clarified and the proteins involved in the uptake and selective retention of alpha-tocopherol discovered. Precise cellular functions of alpha-tocopherol that are independent of its antioxidant/radical scavenging ability have been characterized in recent years. At the posttranslational level, alpha-tocopherol inhibits protein kinase C, 5-lipoxygenase and phospholipase A2 and activates protein phosphatase 2A and diacylglycerol kinase. Some genes (e. g. scavenger receptors, alpha-TTP, alpha-tropomyosin, matrix metalloproteinase-19 and collagenase) are modulated by alpha-tocopherol at the transcriptional level. alpha-Tocopherol also inhibits cell proliferation, platelet aggregation and monocyte adhesion. These effects are unrelated to the antioxidant activity of vitamin E, and possibly reflect specific interactions of alpha-tocopherol with enzymes, structural proteins, lipids and transcription factors. Recently, several novel tocopherol binding proteins have been cloned, that may mediate the non-antioxidant signaling and cellular functions of vitamin E and its correct intracellular distribution. In the present review, it is suggested that the non-antioxidant activities of tocopherols represent the main biological reason for the selective retention of alpha-tocopherol in the body, or vice versa, for the metabolic conversion and consequent elimination of the other tocopherols. Clin Dev Immunol Mar;11(1):13-21.Related Articles, Links Suppression of leukotriene B4 generation by ex-vivo neutrophils isolated from asthma patients on dietary supplementation with gammalinolenic acid-containing borage oil: possible implication in asthma. Ziboh VA, Naguwa S, Vang K, Wineinger J, Morrissey BM, Watnik M, Gershwin ME. Division of Rheumatology, Allergy and Clinical Immunology, Department of Dermatology, University of California at Davis School of Medicine, TB 192, Davis, CA 95616, USA. Dietary gammalinolenic acid (GLA), a potent inhibitor of 5-lipoxygenase (5-LOX) and suppressor of leukotriene B4 (LTB4), can attenuate the clinical course of rheumatoid arthritics, with negligible side effects. Since Zileuton, also an inhibitor of 5-LOX, attenuates asthma but with an undesirable side effect, we investigated whether dietary GLA would suppress biosynthesis of PMN-LTB4 isolated from asthma patients and attenuate asthma. Twenty-four mild-moderate asthma patients (16-75 years) were randomized to receive either 2.0 g daily GLA (borage oil) or corn oil (placebo) for 12 months. Blood drawn at 3 months intervals was used to prepare sera for fatty acid analysis, PMNs for determining phospholipid fatty acids and for LTB4 generation. Patients were monitored by daily asthma scores, pulmonary function, and exhaled NO. Ingestion of daily GLA (i) increased DGLA (GLA metabolite) in PMN-phospholipids; (ii) increased generation of PMN-15-HETrE (5-LOX metabolite of DGLA). Increased PMN-DGLA/15-HETrE paralleled the decreased PMN generation of proinflammatory LTB4. However, the suppression of PMN-LTB4 did not reveal statistically significant suppression of the asthma scores evaluated. Nonetheless, the study demonstrated dietary fatty acid modulation of endogenous inflammatory mediators without side effects and thus warrant further explorations into the roles of GLA at higher doses, leukotrienes and asthma. Prostaglandins Leukot Essent Fatty Acids Jun;70(6):521-8.Related Articles, Links     Spice phenolics inhibit human PMNL 5-lipoxygenase. Prasad NS, Raghavendra R, Lokesh BR, Naidu KA. $$$Department of Biochemistry and Nutrition, Central Food Technological Research Institute, Mysore , India. A wide variety of phenolic compounds and flavonoids present in spices possess potent antioxidant, antimutagenic and anticarcinogenic activities. We examined whether 5-lipoxygenase (5-LO), the key enzyme involved in biosynthesis of leukotrienes is a possible target for the spices. Effect of aqueous extracts of turmeric, cloves, pepper, chili, cinnamon, onion and also their respective active principles viz., curcumin, eugenol, piperine, capsaicin, cinnamaldehyde, quercetin, and allyl sulfide were tested on human PMNL 5-LO activity by spectrophotomeric and HPLC methods. The formation of 5-LO product 5-HETE was significantly inhibited in a concentration-dependent manner with IC(50) values of mg for aqueous extracts of spices and microM for active principles, respectively. The order of inhibitory activity was of quercetin>eugenol>curcumin>cinnamaldehyde>piperine>capsaicin>allyl sulfide. Quercetin, eugenol and curcumin with one or more phenolic ring and methoxy groups in their structure showed high inhibitory effect, while the non-phenolic spice principle allyl sulfide showed least inhibitory effect on 5-LO. The inhibitory effect of quercetin, curcumin and eugenol was similar to that of synthetic 5-LO inhibitors-phenidone and NDGA. Moreover, the inhibitory potency of aqueous extracts of spice correlated with the active principles of their respective spices. The synergistic or antagonistic effect of mixtures of spice active principles and spice extracts were investigated and all the combinations of spice active principles/extracts exerted synergistic effect in inhibiting 5-LO activity. These findings clearly suggest that phenolic compounds present in spices might have physiological role in modulating 5-LO pathway. Thromb Res. 2003;111(4-5): Related Articles, Links   Effective anti-platelet and COX-1 enzyme inhibitors from pungent constituents of ginger. Nurtjahja-Tjendraputra E, Ammit AJ, Roufogalis BD, Tran VH, Duke CC. Herbal Medicines Research and Education Center, Faculty of Pharmacy, University of Sydney, NSW 2006, Australia. BACKGROUND: Based on recent studies, pungent constituents of ginger (Zingiber officinale) and related substances represent a potential new class of anti-platelet agents. The ability of 20 pungent constituents of ginger and related substances to inhibit arachidonic acid (AA) induced platelet activation in human whole blood was studied. METHODS: Anti-platelet activity of the compounds was measured in vitro by the Chrono Log whole blood platelet aggregometer. Molecular hydrophobicity (log P) was measured by reversed-phase high-performance liquid chromatography. COX-1 (ovine) inhibitory effect of [8]-paradol and analogues 1 and 5 was carried out using a COX-1 inhibitor assay kit. RESULTS: [8]-Gingerol, [8]-shogaol, [8]-paradol and gingerol analogues (1 and 5) exhibited anti-platelet activities with IC(50) values ranging from 3 to 7 microM, whilst under similar conditions the IC(50) value for aspirin was 20+/-11 microM. The COX-1 inhibitory activity of [8]-paradol (IC(50)=4+/-1 microM) was more potent than the gingerol analogues (1 and 5) (IC(50) approximately 20 microM). CONCLUSION: The above findings show that gingerol compounds and their derivatives are more potent anti-platelet agents than aspirin under the conditions described in this study. [8]-Paradol, a natural constituent of ginger, was found to be the most potent COX-1 inhibitor and anti platelet aggregation agent. The mechanism underlying AA-induced platelet aggregation inhibition may be related to attenuation of COX-1/Tx synthase enzymatic activity. Lastly, important features of phenolic compounds for inhibition of AA-induced platelet aggregation and COX-1 activity were revealed in this study. J Appl Genet. 2004;45(4): Related Articles, Links   Inhibition of cyclooxygenase-2 by diallyl sulfides (DAS) in HEK 293T cells. Elango EM, Asita H, Nidhi G, Seema P, Banerji A, Kuriakose MA. Department of Molecular Biology, Amrita Institute of Medical Sciences and Research Center, Amrita Vishwa Vidhyapeetam (Deemed University), Cochin Kerala, India. Cyclooxygenase (COX) is involved in modulating inflammatory response through the synthesis of prostaglandins. The inducible isoform of the enzyme, COX-2, is overexpressed in some malignant and premalignant lesions. Several preclinical and clinical studies have reported COX-2 inhibition as an effective strategy for chemoprevention. Nonsteroidal anitinflammatory drugs (NASIDs) such as celecoxib, are the most widely investigated COX-2 inhibitors. The oil-soluble diallyl sulfides (DAS) include monosulfides (DAMS), disulfides (DADS) and trisulfides (DATS). They were found to be effective against canine and human tumors, the mechanism of which remains unresolved. We attempted a comparative evaluation of the antiproliferative effect of DAS in HEK 293T cells. The cells were treated with increasing concentrations of DAMS, DADS and DATS. There were significant differences between the IC50 values of DAMS, DADS and DATS. RT-PCR was performed and the expression of COX-2 was compared with that of b actin. DATS inhibited COX-2 gene expression significantly stronger than DAMS and DADS. The data are suggestive of antineoplastic effect of DAS, mediated by controlling COX-2 expression. Mol Psychiatry. 2002;7(8): Related Articles, Links   Chronic lithium downregulates cyclooxygenase-2 activity and prostaglandin E(2) concentration in rat brain. Bosetti F, Rintala J, Seemann R, Rosenberger TA, Contreras MA, Rapoport SI, Chang MC. Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 10 Rm. 6N202, Bethesda, MD 20892, USA. Rats treated with lithium chloride for 6 weeks have been reported to demonstrate reduced turnover of arachidonic acid (AA) in brain phospholipids, and decreases in mRNA and protein levels, and enzyme activity, of AA-selective cytosolic phospholipase A(2)(cPLA(2)). We now report that chronic lithium administration to rats significantly reduced the brain protein level and enzyme activity of cyclooxygenase-2 (COX-2), without affecting COX-2 mRNA. Lithium also reduced the brain concentration of prostaglandin E(2) (PGE(2)), a bioactive product of AA formed via the COX reaction. COX-1 and the Ca(2+)-independent iPLA(2) (type VI) were unaffected by lithium. These and prior results indicate that lithium targets a part of the AA cascade that involves cPLA(2) and COX-2. This effect may contribute to lithium's therapeutic action in bipolar disorder PGH2 Prostaglandin E1 Utvider blodkar Hemmer blodproppdannelse Senker blodtrykket Hemmer kolesterolsyntese Demper inflammasjon Prostaglandin E2 Øker LH Øker følsomheten i livmorens nerveender Fremmer blodproppdannelse Utvider blodkar Øker følsomhet i smertereseptorer Fremmer inflammasjon Prostaglandin F2d Sammentrekning av glatte muskler, livmor, blodkar → menstruasjonssmerter Prostaglandin I2 Hemmer blodpropp- Dannelse Utvider blodkar Tromboksan A2 Sammentrekker blodkar Fremmer blodpropp- dannelse (koagulasjon?) Leukotrien C,D,E Fremmer inflammasjon Prostaglandin E3 Hemmer vekst av Kreftceller Hemmer blodpropp- dannelse Hemmer åreforkalkning Demper inflammasjon Prostaglandin E4

58 Postprandial inflammation
60% of the day we are in a postprandial state. It is very important to consider the postprandial metabolic and hormonal effect of food and its relation to inflammation. Postprandial inflammation is an independent factor in evaluating food quality. The quality and quantity of fatty acids and the glycemic index in a meal are major determinants of the magnitude of postprandial inflammation. (Margioris, 2009) Most proinflammatory: red meat and potatoes/rice/pasta Least proinflammatory: fish and vegetables

59 Ofte e. kronisk forhøyet blodsukker etter måltider og hjertesykdom
toksisk på insulinproduserende celler og nedsetter insulinvirkningen (glukose toksisitet, Rossetti, 1990) opp til dobling av risiko for dødelighet av hjertesykdom (Honolulu Heart Study, Whitehall Study) Blodsukker etter måltider men ikke fastende blodsukker er en uavhengig risikofaktor for hjerteinfarkt og kardiovaskulær mortalitet (Diabetes Intervention Study, Hanefeld 1997 og DECODE study 1999) økt oksidativt stress, bl.a. glykosylering og oksidering av LDL kolesterol etter måltider (Ceriello 1999)

60 Konsekvenser av høyt insulin ved faste og etter måltider
økt risiko for hjertesykdom (Helsinki Policemen Study (Pyorala 2000) bedre indikator av dødelighet av hjertesykdom enn hyperglykemi (Paris Prospective Study, Fontbonne 1991) fastende serum insulin kraftig markør for økt kardiovaskulær risiko (Quebec Cardiovasculart Study, Despres 1996) Økt intracellulær dannelse av frie radikaler og økt insulinresistens (Ceriello 1995, Paolisso 1996)

61 Insulinresistens syndrom
høyt insulin selv ved faste mavefedme type 2 diabetes hjerte- og karsykdom høyt blodtrykk lavt HDL kolesterol og høye triglyserider høy urinsyre mikroalbuminuri PCO og infertilitet hos kvinner

62 Insulinresistens og Inflammasjon
Overvekt og insulinresistens er proinflammatoriske tilstander Inflammasjon: fellesnevner ved nesten all sykdom inkl. PCO, abort, svang.dia, preeklampsi Inflammasjon: eikosanoidubalanse har sentral rolle

63 Kroppsvekt, energirestriksjon og inflammasjon
Pos. korrelasjon mellom vekt og inflammasjon Vektreduksjon redusert inflammasjon reduserte symptomer ved RA, OA, psoriasis mm. Effektivt med fysisk aktivitet og kaloriredusert diett ved OA

64 Obesity- an inflammatory disease (1)
Pathological increase in body fat mass Genetic componenty contributes to worsening this phenomenon Cytokines produced by adipocytes and other adipose tissue cells (preadipocytes and macrophages)

65 Obesity- an inflammatory disease (2)
Preadipocytes: Present from birth and give rise to new adipocytes Contribute to normal or abmormal fat development Share fundamental characteristics with the macrophage (important in inflammation, immunity and cellular remodelling). Leptin is increased in obesity and stimulates recruitment of macrophages in adipose tissue Leptin induces TNF-a, IL-6 and CRP Result: Mild chronic systemic inflammation, altered lipid metabolism Adiponectin has opposite effects to those of adipocytokines (leptin, IL6, TNF-a etc.) Adiponectin is low in obesity and increases with weight loss

66 Obesity- an inflammatory disease (3)
Chronic inflammation underlies both obesity and the metabolic syndrome Measured by increased hs-CRP, leptin, low adiponectin Seen already in very young obese children in association with many features of the metabolic syndrome. Increased TNF-a and IL6 worsen insulin resistance Adiponectin falls and leptin resistance gets established contributing to more insulin resistance. A vicious circle is in place Glucolipotoxicity on the beta cells affect insulin release and increase risk of diabetes Energy regulation is affected by decoupling leptin and insulin signalling in the central nervous system

67 The net effect of obesity the change of the phenotype of adipocytes to pro-inflammatory
Indeed, microarray on dispersed ex vivo adipocytes from non-diabetic but obese Pima Indians showed that at least 52 of inflammation-related genes appear to be upregulated compared to non-obese Pima

68 VLCKD diet (Eurodiet phase 1& 2) changes the expression of multiple genes in ex vivo fat cells
E.g., an increase in the expression of the antiinfammatory cytokine IL10 and the receptor antagonist of IL1 (IL1ra) after 28 days of VLCD

69 Obesity and Inflammation
56 healthy premenopausal obese women (age years, BMI 37.2±2.2, WHR ) and 40 age-matched normal weight women were studied. Obese women had increased basal concentrations of (TNF- , P<0.01), interleukin-6 (IL-6, P<0.01), P-selectin (P<0.01), intercellular adhesion molecule-1 (ICAM-1, P<0.02), and vascular adhesion molecule-1 (VCAM-1, P<0.05).

70 Very low calorie ketogenic diet and inflammation reduction
After 24 wk of consuming hypoenergetic diets either low in carbohydrate, low in fat, or moderate in protein, C-reactive protein (CRP) levels fell by 35, 13, and 15%, respectively McAuley, et al (2005) Diabetologia 48:8-16. Significant reductions in inflammatory markers (hsTNF-, hsIL-6, CRP, and soluble intracellular adhesion molecule-1 (sICAM-1) after consumption of a VLCKD (Eurodiet phase 1 and 2) in overweight men Sharman, M. J. et al. (2004) Clin. Sci. (Lond.) 107:

71 Practical antiinflammatory management in obesity
Initial weight reduction with VLCKD (Eurodiet pase 1 and 2) Long term normalisation of BMI through: -A low glycemic load Mediterranean diet (Eurodiet phase 3 and 4) -Regular physical exercise -Stress and sleep management Monitor inflammation initially and during treatment by measuring hs-CRP, leptin, adiponectin, fasting insulin/C-peptide

72 Cretan Mediterranean Diet: great tasting, low cost treatment without the side effects
Tested and proven by time and 1400 international research studies showing benefits: -288 on heart disease -166 on cholesterol - 97 on obesity - 93 on diabetes - 68 on high blood pressure - 32 on longevity - 15 on Alzheimer’s Disease - 9 on Depression - 3 on Asthma Diet In Greek (DIAITA) means Way of Life

73 Cretan Mediterranean Diet: Live longer and better
-Modified Mediterranean diet and survival: EPIC-elderly prospective cohort study. Trichopoulou A et al BMJ Apr 8 and Public Health Nutr Jun;10(6): Epub 2007 Mar 5 Study on 74,607 healthy European men and women, aged 60 or more CONCLUSION: The Mediterranean diet, modified so as to apply across Europe, was associated with increased survival and 14% reduction of overall mortality . -

74

75 Hippocrates: What’s good for the heart is good for the brain Father of Medicine 460-370 BC

76 Mediterranean Diet

77 Mediterranean Diet cuts Stroke Risk more than Drugs
J Spence Stroke 2006 Sep;37(9):2430-5 Mediterranean diet, which is high in beneficial oils, whole grains, fruits and vegetables, has been shown to reduce stroke and myocardial infarction by 60% in 4 years.This effect is twice that of simvastatin.

78

79 Adherence to Mediterranean Diet eating pattern reduces the risk for Alzheimer’s Disease
- Scarmeas N, et al Mediterranean diet and risk for Alzheimer's disease. Ann Neurol Jun;59(6): - Solfrizzi V, et al Adherence to a Mediterranean dietary pattern and risk of Alzheimer's disease. Ann Neurol Nov;60(5):620; - Panza F, et al Mediterranean diet, mild cognitive impairment, and Alzheimer's disease. Exp Gerontol Jan-Feb;42(1-2):6-7; - Solfrizzi V, et al. Whole-diet approach, Mediterranean diet, and Alzheimer disease. Arch Neurol Apr;64(4):606;

80 And it tastes great !!

81

82 The traditional Mediterranean Diet needs a reform to accommodate today’s lifestyle needs
Lower glycaemic load Emphasis on better essential fat balance

83 The new Mediterranean diet
Low glycemic index/load carbohydrates Rich in omega-3 fatty acids/fish Rich in Olive Oil Fruits, vegetables beans & grains Limited meat intake

84 Proteiner-meget viktig
Proteiner består av aminosyrer Kroppen kan ikke lage alle aminosyrer selv 9 essensielle aminosyrer må inntas med maten Vi trenger ca. 1-1,2 g protein pr. Kg fettfri kroppsvekt Barn over 2-3 år og tenåringer trenger mer Mosjon øker proteinbehovet

85 Proteiner-særlig viktig ved vektreduksjon
Proteiner gir størst metthet Husk å ikke overdrive men spis nok proteiner fra flere kilder til alle måltider og mellommåltider Stabiliserer blodsukkeret

86 Proteiner- hvor finnes de?
Kjøtt, fjærfe, fisk Egg (mest i eggehvite) Soyabønner Inneholder ikke alle aminosyrer: Nøtter og frø Belgfrukter Kornvarer

87 Alle karbohydrater er ikke like
Fører til variabel blodsukker- og insulinstigning avhengig av: Rask eller langsom nedbrytning i mavesekk og tarm Lavt eller høyt fiberinnhold Samtidig fett- eller proteininntak

88 Glykemisk indeks (GI) Rangeringsmetode for matvarer
Basert på deres effekt på blodsukkerstigning Høy glykemisk indeks er ugunstig Lav glykemisk indeks er gunstig

89 Glycemic Load (Glykemisk belastning)
Formel for beregning av Glykemisk belastning: GI x Karbohydratinnhold/100g Tar hensyn til både glykemisk type og mengde karbohydrat Eksempler: Matvarer GI GB/100g Glukose Sukker 68 68 Bagett 95 48 Bakt potet 85 17 Corn flakes Surdeigsbrød 54 25 Spagetti 39 10 Kikerter 28 6 Linser 26 3

90 2000 Kcal / dag Offisielle kostanbefalinger: GB 135
Mat for livet: GB 35

91 Feil å fokusere bare på gram karbohydrat eller fett
MATVARENES OG KOSTENS KVALITET ER VIKTIGST

92 Fett- ikke ett fett? -Transfett er skadelig (herdet vegetabilsk fett) -Margariner og raffinerte oljer fra soja, mais og solsikke bør unngås, de er sterkt bearbeidet og bidrar med for mye omega 6 fett som kan herske ogfremmekroniske betennelser -”Mettet fett” og “meierifett” har vært omdiskutert, men grundig gjennomgang av forskning viser at mettet fett ikke er forbundet med økt eller redusert risiko for hjertesykdom Melkefett minsker risiko med 6-9%. Kokosfett virker også svakt positivt. Mettet fett som ledd i et variert kosthold er kun problematisk BARE SAMMEN MED HØYKARBOHYDRAT KOSTHOLD - Fettfattig kost bør frarådes - Fokus på sunt fett fra flere kilder: Nøtter, frø, fet fisk, avokado, olivenolje, rapsolje, smør, oster, kokosfett

93 Fett- ikke ett fett? - Fettfattig kost bør frarådes
Fokus på sunt fett fra flere kilder: Nøtter, frø, fet fisk, avokado, olivenolje, rapsolje, smør, oster, kokosfett Mens mettet fett har en nøytral effekt på risiko for hjertesykdom og meieriprodukter reduserer med 6-9% får du hhv 30% og 20% risikoreduksjom av nøtter og olivenolje, fet fisk og hele 68% risikoreduksjon ved å følge middelhavskosten (Mente, 2009)

94 Omega 3 og 6 fettsyrebalanse for god helse
Både omega 3 og 6 livsviktig og må inntas med maten For mye omega 6 øker betennelsestilstander Nok omega 3 demper betennelser Vestlig kosthold gir ganger mer omega 6 enn 3 Ideelt burde vi innta 2 ganger mer omega 6 enn 3 Nå kan man lett få målt sin egen omega 3:6 balase gjennom blodprøve

95 Modern low GL Mediterranean Diet
Sugar, fine bread, refined wheat flour, potato High GL Zero GL Nuts, rapeseed oil, olive oil, fatty fish Medium GL Pasta, brown rice, unprocessed cereal products Modern low GL Mediterranean Diet Zero GL Protein: fish, chicken, meat, game, eggs, low fat-fermented dairy prod. Low GL Vegetables, pulses, fruit, berries

96 The Detrimental Effects of Sleep Deprivation
Even modest sleep deprivation markedly increases inflammatory cytokines. This finding helps explain why pain flare-up occurs in response to lack of sleep in a variety of disorders. In this carefully controlled study, sleep deprivation caused a 40% to 60% average increase in the inflammatory marker IL-6 in men and women, while men alone showed a 20% to 30% increase in TNF-a. Both IL-6 and TNF are potent pro-inflammatory cytokines that induce systemic inflammation (Vgontzas et al. 1999; Vgontzas et al. 2001).

97 Stress and inflammation
Stress is an adaptive response common to all living organisms. It involves the activation of the corticotrophin releasing factor (CRF) releasing pathway. The CRF pathway response stimulates over-activity of immunological chemicals. (De Giorgio R, Gastroenterology 1996;110). There is a link between stress and an overactive inflammatory response. Individuals with major depression were shown to have an exaggerated inflammatory response to psychological stress in comparison to those who do not have depression. (Sep. 1, 2006 issue of the American Journal of Psychiatry)

98 Vitamin D deficiency and inflammation
 Increased concentrations of serum TNF-α, an inflammatory marker, were found in women who had insufficient vitamin D levels. Inverse relationship between vitamin D levels and concentrations of TNF-α in a healthy, non-diseased population. (Peterson 2008) This may explain the vitamin's role in the prevention and treatment of inflammatory diseases, including heart disease, multiple sclerosis and rheumatoid arthritis. "Adequate vitamin D levels identified in this study are consistent with recent research that suggests the DRI should be increased.”

99 Vitamin D deficiency and inflammation
  To improve vitamin D status and achieve its related health benefits, most people should get at least 1000 IU of vitamin D per day. Exposing 25 percent of the skin's surface area to 10 minutes of sunlight three days per week will maintain adequate levels in the majority of people; however, people with darkly-pigmented skin need more. Only a few foods contain vitamin D naturally, such as fatty fish; other sources are dietary supplements and vitamin-D-fortified foods, including some milk Optimal blood levels of Vitamin D year round: nmol/l (normal range nmol/l)

100 Get enough sunshine- Slash risk for heart disease?
Study presented at American Heart Association meeting by Dr. Tami Bair and Dr. Heidi May, of the Intermountain Medical Center in Utah people studied for 13 months. Risk of heart attack, stroke, congestive heart failure and death are dramatically associated to Vitamin D deficiency. People with low levels (< 37,5 nM) had a 45% increased risk for cardiovascular disease, 78% greater risk of stroke and double the risk for congestive heart failure, not to mention a 77% increased risk of death, compared to people with Vitamin D levels > 75 nM Get tested and get enough Vitamin D to reach nM year round. Expose large part of body to sun 10min daily WITHOUT sun blocker, then use protection if you stay longer.

101 Physical Activity and Inflammation Among Apparently Healthy Middle-aged and Older US Adults
Study subjects were 3638 apparently healthy US men and women 40 years and older. (Abramson, 2002) Results  More frequent physical activity was independently associated with a lower odds of having an elevated C-reactive protein level.Similar associations were seen for white blood cell count and fibrinogen levels. Conclusions  More frequent physical activity is independently associated with a lower odds of having elevated inflammation levels among apparently healthy US adults 40 years and older, independent of several confounding factors. The results suggest that the association between physical activity and reduced coronary heart disease risk may be mediated by anti-inflammatory effects of regular physical activity.

102 The following dietary factors protect against inflammation
High intake of antioxidants (vegetables, fruits, berries, nuts, seeds, herbs, spices, chocolate Soluble fiber (oats, legumes, vegetables) Moderate intake of alcohol and coffee/tea Low glycemic Mediterranean diet (low in sugars and starches) Higher intake of omega 3 (oily fish, flax seed) and monounsaturated plant oils (olive oil, rapeseed, avocado, almonds, macadamias)

103 Antiinflammatory Lifestyle
Follow a low glycemic Mediterrenean Diet (60% plants) Eat enough fatty fish or take omega 3 supplement Exercise regularly (brisk walk > 30min daily) and resistance training 2-3 times weekly Avoid smoking Master stress and sleep well and long enough (7-8 hours) Get enough sunshine or consider Vitamin D

104 Oppfølging og veiledning er nøkkelen for å lykkes
Kyndig veiledning og oppfølging er svært viktig for mange Kunnskap er en forutsetning, men ikke nok. Motivasjon og mestring over tid er viktigst.

105 Mestring av livsstilsendring
Det dreier seg om å skrive med motsatt hånd

106 Opprettholdelse av vekttapet med oppfølging (n =180)
Larocque & Gougeon, 1999 % Opprettholdelse av vektapet 20 40 60 80 100 1 2 3 4 Med oppfølging Uten oppfølging Lengde for studiene (år) Ref. The American Journal of Bariatric Medicine. Fall Vol.14 n 3.

107 Mange veier fører til Roma
Det viktigste er å faktisk nå målet på en sunn måte

108 Individualisering Unngå ”one size fits all”- Individualisering er viktig, bade av hensyn til genetiske forskjeller, men også preferanser, familiære, sosioøkonomiske faktorer, smak

109 Hvordan jobber vi på dr. Lindbergs klinikker?

110 Mat Mosjon Mestring Medikamenter

111 Dr. Lindbergs Klinikker i 4 norske byer
Klinikken har behandlet over pasienter fra hele Norge og har avdelinger i Oslo, Bergen, Stavanger og Arendal leger Fedon Lindberg, indremedisiner Elisabet Ottesen Trude Hetland Brynjulf Barexstein Paal Norheim Dela Kamyab Mohsen Zangani Ernæringsterapeuter/Sykepleiere Hege Barhaughøgda, diabetes s.pl. / kostveileder Merete Frafjord, sykepleier/ kostveileder Ann-Kristine Rolland, ernæringsfysiolog Anna Ingwardo, ernæringsfysiolog Lotte Evenstad, sykepleier

112 Dr. Fedon Lindbergs Klinikk
Behandling / forebygging av overvekt, det metabolske syndrom og livstilsrelaterte sykdommer Tverrfaglig Helhetlig Høy faglig kompetanse Individuelt / grupper Fokus på livsstilsendring Positiv ernæring Hjelp til mestring Mosjonsveiledning

113 Behandlingstilbud Spesialisert på: Det metabolske syndrom
Insulinresistens Diabetes Overvekt

114 Behandlingstilbud Ernærings - og livsstilsendring ved:
Mage- / tarmsykdommer Hjertesykdom Høyt blodtrykk Høyt kolesterol Migrene PCO ( polycystisk ovariesyndrom ) Menstruasjonsforstyrrelser / Fertilitetsproblemer / Svangerskap Astma og allergi Psoriasis og eksem Muskel- / leddplager Fibromyalgi og kronisk utmattelses syndrom Betennelsestilstander

115 Behandlingsforløp Legen rekvirerer blodprøver
Pasienten bestiller time hos behandler – vanligvis hos lege først (60 min ) Legen rekvirerer blodprøver Pasienten tilbake etter 3-4 uker – 30 min Ny legekonsultasjon/gjennomgang av prøver (30-60min) Planlegger videre forløp hos lege / ernæringsterapeut / mestringsterapeut (30 eller 60min)

116 Lager behandlingsopplegg i samarbeid med pasienten!
Kartlegging Individuelle råd, basert på pasientens mål,preferanser, vaner, hverdager og ønsker Sykehistorie Familieanamnese Kostanamnese / Vektanamnese Mosjonsfrekvens/type Adferdsanamnese (livsvaner, søvn, forhold, stressmestring, prioriteringer, avhengighet) Blodprøver Impedansevekt Lager behandlingsopplegg i samarbeid med pasienten!

117 Kartlegging Pasienten får tilsendt detaljert spørreskjema inkl. 3 dagers kostregistreringsskjema som fylles ut og tas med under første konsultasjon Under konsultasjonen benyttes elektronisk journalmal inkl. bioimpedanse måling - SWOT analyse (personlige styrker, svakheter, eksterne muligheter og trusler) - Personlig målsetningsskjema (S.M.A.R.T. prinsippet) - Personlig prioriteringsskjema Avhengig av problemstillingen fylles ut TFEQ (Three Factor Eating Questionnaire) og/eller SL90-R (Kartlegging av problem og mestring), MADRS etc.

118 Behandlerpakke- Strukturert oppfølging
Ett års oppfølging En hel time (60min) og to halve timer (30min hver) hos lege, en hel time og fem halve timer hos enten diabetessykepleier eller ernæringsfysiolog. Pris kr: 6590,- (Ordinær pris: 7180,-) Ved autogiro avtale: kr 549,- pr måned

119 Behandlerpakke- Strukturert oppfølging
Behandlerpakke – Et halvt år En hel time (60min) og en halv time (30min) hos lege, en hel time og to halve timer hos sykepleier / ernæringsfysiolog.   Pris kr: 3920,- (ordinær pris: 4620,-) Ved autogiro avtale: kr 560 pr måned

120 Eurodiet Kurs for medisinsk behandling av overvekt /fedme
Gruppesamlinger og individuelle konsultasjoner. Mestring og motivasjon vektlegges. Passer for deg med en BMI › 30, eller BMI › 27 med tilleggssykdom relatert til overvekt, som for eksempel høyt blodtrykk, diabetes, høyt kolesterol, slitasjegikt, søvnapné med mer. Fire gruppesamlinger og tre individuelle konsultasjoner à 30min hver. Kursene holdes av kvalifiserte sykepleiere og ernæringsfysiologer ved Dr Fedon Lindbergs klinikk. Pris kr: 4000,- ( Eurodiet matvarer til bruk i behandlingen kommer i tillegg )

121 Veldokumentert metode for vektreduksjon under obligatorisk medisinsk oppfølging
På det internasjonale markedet siden 1990, I Norge siden 2000 Grunnprinsipper: Personlig ernæringstilpasning Atferdsendring Medisinsk oppfølging Gradvis overgang til sunt kosthold – ” kost og vekt i balanse” Trygg og effektiv metode for vektreduksjon ved sykelig overvekt (BMI>30) Karbohydratfattige, fettfattige og høyverdige - proteinprodukter Inndelt i 4 faser over ca 8 mnd

122 Dr. Fedon Lindbergs øvrige aktiviteter
Forfatter/foredrag: Kunnskap og inspirasjon for endring av livsstil 10 bøker om kosthold- og livsstilsendring Matvarer: Sunne, nyttige og velsmakende lavglykemiske matvarer.

123 Utgitt 14 bøker i Norge Vekt Helse

124

125 Oversatt til 14 språk og utgitt i 20 land og 5 kontinenter
Published in: UK, Ireland, Australia, New Zealand, Mexico/South America, Brazil, Portugal, Poland, Norway, Sweden, Finland, Denmark, Greece. To be published in 2007 in USA, Germany, Holland and Israel

126 Kostreform i Norge 1 av 4 nordmenn (23%) har endret kostvaner de siste årene som resultat av nye kostholdsråd og kostholdsdebatten. 12,9% følger Fedon Lindbergs kostholdskonsept. Gjennomnsittlig sukkerforbruk i Norge har minsket fra 43 til 35 kg per år siden 2000 Men Norge er fortsatt på siste plass i Europa i grønnsaksspising Av de 23 % som har endret kostvaner: 9 av 10 spiser mer frukt og grønnsaker 3 av 4 mindre fett 3 av 4 mindre sukker 63 % mer hvitt kjøtt som kylling 65 % mer fisk 44 % mindre brød/poteter/pasta Norsk Gallup for TV2, februar 2004

127 Hvor godt har vi egentlig av myter?

128 Helse er ikke lenger under statlig kontroll
Folkebevegelse, men også sterk påvirkning av media, reklame fra store industrielle aktører, dagligvarehandelen, pris og tilgjengelighet

129 Avslutningskommentarer
Fettinntaket i likhet med all annen mat bør være variert. Smør er Ok, men neppe optimal som eneste, eller største fettkilde. Ny studie: Lavglykemisk middelhavskost ”kurerte” 32% med insulinresistens på 12 uker! Lavkarbo med mest rødt kjøtt økte generell dødelighet, mens lavkarbo med stort innslag av vegetabilsk protein/fett (nøtter, frø) reduserte risiko for kreft og hjertesykdom og dødelighet av alle årsaker (Harvard Univ. Fung 2010) Mye, men ikke alt kan bli bedre ved å redusere karbohydrat Høyt blodsukker og insulin kan forklare en del, men langt fra alt, ikke minst når det gjelder inflammasjon Kjøtt, fisk, kylling, egg øker insulin i vesentlig grad, men ikke blodsukkeret. Mye tyder på at det er kombinasjonen av høyt blodsukker og insulin som er problematisk

130 Avslutningskommentarer
Ingen eier sannheten. ”En ting vet jeg at jeg intet vet” (Sokrates) ”Gjør det så enkelt som mulig, men ikke enklere enn det” (A. Einstein) ”En ny tanke går gjennom tre stadier: Først blir den latterliggjort, så motarbeidet, til den til slutt blir en selvfølge” (A. Schoppenhauer) Mennesker er ikke like. Man må akseptere at ikke et kosthold er bra for alle ”Alt kan være giftig. Det er dosen som avgjør” (Paracelsus) Man må tenke helhetlig ift livsstil. Hygge, gode relasjoner, stress-mestring, nok søvn og fysisk aktivitet har enorm betydning Kan man følge lavkarbokosthold hele livet og få hjertesykdom eller kreft? Ja, men man reduserer risikoen Mest mulig mat uten tilsetningsstoffer (hva med bacon og nitritter/nitrater?) Måtehold, måtehold, måtehold

131 Best mulig helse - færrest mulig medikamenter - Ta kontakt med Klinikken vår
Tel

132 Kost i balanse- for et bedre liv


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