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• Wer ist Dr. Barry Sears ?

• www.DrSears.com

• Welche Rolle spielt Fischöl in der Menschheitsgeschichte ?

Fettsäuren

• Einfach-ungesättigte Fettsäuren ( flüssig bei Raumtemperatur – wenige

Doppelbindungen)• Mehrfach-ungesättigte Fettsäuren ( flüssig im Kühlschrank – viele

Doppelbindungen)• Gesättigte Fettsäuren ( fest bei Raumtemperatur )

Eicosanoide

• Eicosa = Zwanzig für 20 C-Atome in einer Reihe• 1936 von Ulf van Euler entdeckt-• Genannt Prostaglandine weil aus der Prostata

isoliert• Z.Zt. > 100 verschiedene Eicosanoide bekannt• 1982 Dr. J.R. Vane, Dr. Samuelsson und Dr.

Bergstrom bekommen den Nobelpreis in Medizin für ihre Arbeiten über Eicosanoide

Eicosanoide: Eigenschaften

• „ Second messenger“

• Rezeptoren für Eicosanoide in der Zellwand

• Bestimmen die Wirkung auf cAMP

• „gute“ Eicosanoide cAMP

• „schlechte“ Eicosanoide cAMP

Linolsäure 18:2w6

Eine Omega 6 - -Fettsäure

Gamma Linolsäure (GLA)

18:3w6 18 Carbon, 3 Doppel -

bindungen, eine Omega 6 FS

Di -homo Gamma Linolsäure

(DGLA) 20:3w6

(verlängert Carbonkette)

Delta 6 Desaturase

Gehemmt durch Alkoholüberschuss,Virus

Alphalinolsäure (ALA)

Elongase

Arachidonsäure (AA)

20:4w6 Delta 5 Desaturase

Aktiviert durch Insulin

gehemmt durch Eicopentaeonsäure=EPA,

Glucagon COX

Gute Eicosanoide PGG1; PGH1 Effekte von PGE1:

Unterdrückt Insulinfreisetzung Erweitert Blutgefässe Verhindert Thrombozytenverklumpung Erhöht das menschliche Wachstumshormon Erhöht die Lymphokinfreisetzung Senkt Cholesterol Senkt Histamin Reduziert Schmerz Reduziert Entzündung Senkt Schlafbedürfnis Senkt Magensäure Wirkt als Bronchodilatator

Schlechte Eicosanoide

COX (Cycloxygenase)

PGE 2

Hydroxylierte Fettsäuren

12 -15 Lipoxygenase

5 Hydroxyeicosa - Tetranoide

(5 -HETE, 5 HETE Lacton)

5 -Lipoxygenase

Leukotriene (LTB4)

Die Eicosanoid Stoffwechselwege

Eicosanoide

• „ Schlechte“ Eicosanoide ( Arachidonsäure = AA = langkettige Omega 3 Fettsäure)

• „Gute “ Eicosanoide ( Eicopentaeonsäure = EPA=langkettige Omega 3

Fettsäure) Ratio AA/EPA: 1,5 – 3 ideal 10 es drohen chron. Erkrankungen 15 oder höher bei chron. ErkrankungenTriglyceride/HDL: 1 ideal ; 2 gut

Die Diät nach Dr. Barry Sears

• Die ausgewogene Protein- und Kohlehydratzufuhr bei jeder Mahlzeit

• Die Reduktion von Kalorien ohne Hungergefühl und Entsagung

• Zufuhr von Fischöl

Insulin und Eicosanoide

• Insulin stimuliert die Cholesterolproduktion in der Leber

• Weniger Insulin – weniger „ schlechte“ Eicosanoide – weniger Cholesterol

• „ gute“ Eicosanoide senken den Insulinspiegel

• Wichtig: die Kontrolle des Insulinspiegels

Der Sears Teller

1/3 Proteine

2/3 Kohlehydrate

1 Teelöffel einfach ungesättigtes Fett

Welche Proteine ? Welche Kohlehydrate ? Welches Fett ?

• Protein : Gut = Fisch, Hähnchen,Truthahn,Schweinefleisch mit wenig Fett

• Kohlehydrate: Gut = Gemüse,

Früchte,ausgesuchtes Getreide (Hafer, Gerste )

Schlecht: Stärke und das meiste Getreide

( Brot,Nudeln, Reis,Kartoffeln )

Fett: Gut = Olivenöl, Avocados

Schlecht = Milch, Margarine, Sojaöl; Sonnenblumenöl

Fischöl - Dosierung

• Erhaltungstherapie = 2,5 Gramm/Tag=1 Teelöffel oder 4 Kapseln

• Verbesserung der Herz-Kreislaufsituation:

2,5-5 Gramm/Tag=1-2 Teelöffel oder 4-8 Kapseln• Verbesserung der Hirnleistung und Reduktion von

Entzündung:

5-10 Gramm/Tag=2-3 Teelöffel oder 8-16 Kapseln• Zur Behandlung von neurologischen

Erkrankungen: 10-25 Gramm/Tag ( 1-3 Eßlöffel )

Qualität von Fischölprodukten

• Kriterien:

• 1. Gesamtmenge an langkettigen Omega 3 Fettsäuren > 60 % aller Fettsäuren

• 2. Quecksilbergehalt < 10 ppb

• 3. PCB < 30 ppb

• 4. Dioxine < 1 ppt

Stiftung Warentest 8/05

• Aldi Lachsölkapseln 500 mg

• 120 Stück 3 Euro

• Dm/Das gesunde Plus Omega-3 Lachsöl 1000

• 60 Stück 3 Euro 95

Omega-6 fatty acids cause prostate tumor cell growth in culture; potential new drug target identified, as well August 1, 2005. A study conducted at the San Francisco VA Medical Center (SFVAMC) has demonstrated that omega-6 fatty acids such as the fat found in corn oil promote the growth of prostate tumor cells in the laboratory. The study also identifies a potential new molecular target for anti-tumor drugs: an enzyme known as cPLA2, which plays a key role in the chain leading from omega-6 fatty acids to prostate tumor cell growth. The study was led by Millie Hughes-Fulford, PhD, director of the Laboratory of Cell Growth at SFVAMC and scientific advisor to the U.S. Undersecretary of Health for the Department of Veterans Affairs. It is being published in the September 2005 issue of Carcinogenesis, and is currently available online. Working with human prostate cancer cells in tissue culture, Hughes-Fulford and her fellow researchers identified for the first time a direct chain of causation: When introduced into prostate tumor cells in culture, omega-6 fatty acid causes the production of cPLA2, which then causes the production of the enzyme COX2. In turn, COX2 stimulates the release of PGE2, a hormone-like molecule that promotes cell growth. "What's important about this is that omega-6 fatty acids are found in corn oil and most of the oils used in bakery goods," says Hughes-Fulford, who is also an adjunct professor of medicine at the University of California, San Francisco (UCSF). "Which means that if you're eating a diet high in omega-6 fatty acids, it's possible that you're turning on this cancer cascade, which has been shown to be a common denominator in the growth of prostate, colorectal, and some breast cancers." The study points out that 60 years ago in the United States, the dietary ratio of omega-6 to omega-3, a beneficial fatty acid, was 1 to 2. Today, the ratio is 25 to 1. Over that same 60 years, the incidence of prostate cancer in the U.S. has increased steadily. Hughes-Fulford also found that flurbiprofen, a non-steroidal anti-inflammatory drug commonly prescribed for arthritis, blocked the production of cPLA2 and broke the chain leading to cell growth. This means, she says, that new drugs might be developed that could specifically target cPLA2 and prevent COX2 from being released. "COX2 has been implicated in the growth of many types of tumors," she notes. "So if you can find a way to block that cascade in the tumor, starting with cPLA2, you might have a new way of modifying or slowing tumor growth." Hughes-Fulford points out that cPLA2 inhibitors would avoid the problems inherent in the class of drugs known as COX2 inhibitors. These drugs have been shown to be effective against tumor growth as well as in treating the pain associated with inflammatory conditions such as arthritis, but have been implicated in increased risk of cardiovascular problems in people who take them regularly. "COX2 inhibitors also inhibit prostacyclins, which are enzymes that are beneficial to the heart, and cPLA2 inhibitors would not affect those," she explains. In future research, Hughes-Fulford will be looking at the overall effect of different types of fatty acids on different tumor types in cell lines as well as human biopsies. She plans a study that will correlate type of fatty acid with tumor stage and grade in order to obtain a clearer picture of specific effects of different fats on tumor progression. Co-authors of the study were Raymond R. Tjandrawinata, PhD, of UCSF, Chai-Fei Li, BA, of SFVAMC, and Sina Sayyah, BA, of SFVAMC and UCSF. The research was funded by awards from the U.S. Department of Veterans Affairs and in part by grants from the National Aeronautics and Space Administration. Funding was administered by the Northern California Institute for Research and Education (NCIRE).  

Low Fat Diet Slows Growth of Prostate Cancer Cells

"Blood from men who had undergone the low-fat group significantly reduced in vitro growth of LNCaP cells compared to Western diet serum."

May 18, 2005 – A high-fat diet and sedentary lifestyle may predispose men to develop prostate cancer through changes in serum hormones and growth factors. In a previous study, researchers from University of California, Los Angeles and Baltimpor, MA. showed that blood drawn from men who were limited to a low-fat diet and were exercising reduced serum-stimulated growth of prostate cancer cells ina dish. At the American Urological Association annual meeting this past May, the same research team presented results of another study they designed to see whether a low-fat vs Western diet affects the blood supply's impact on prostate cancer growth. This study involved men with prostate cancer on watchful waiting. They took 18 men with prostate cancer and randomized them to eat either a low-fat (15% calories from fat) or a regular Western (40% calories from fat) diet for 4-weeks. The men's fasting blood was drawn before and after the diet period, and measured for sex hormones, lipids, fatty acids, IGF-I and IGF binding proteins.To make sure the men stuck to the assigned diet, all their meals were prepared at the UCLA Clinical Research Center, with close monitoring by a research dietician. To assess the effect of the diet on prostate cancer growth, LNCaP cells were cultured in the laboratory and bathed in "before" and "after" serum drawn from these 2 groups of 9 men each. ResultsBlood from men who had undergone the low-fat group significantly reduced in vitro growth of LNCaP cells compared to Western diet serum. Serum levels of linoleic acid (omega-6, the predominant fatty acid in the Western diet in baked and fried food) were significantly reduced in the low-fat relative to the Western diet group and positively correlated with serum-stimulated growth. In addition, serum omega-3 fatty acid levels (found in fish oil, predominant in the Asian diet) negatively correlated with serum-stimulated growth. There was a trend for serum IGFBP-1 levels to negatively correlate with serum-stimulated growth in the low-fat group.

Conclusions

In this prospective randomized dietary intervention trial, a low-fat diet resulted in changes in serum fatty acid levels that impacted the growth of human LNCaP cancer cells in a dish.

Further studies are indicated evaluating reducing linoleic acid intake and increasing omega-3 fatty acid intake for prostate cancer prevention and treatment.

GROWTH INHIBITORY EFFECTS OF A LOW-FAT DIET ON PROSTATE CANCER CELLS IN VITRO: RESULTS OF A PROSPECTIVE RANDOMIZED DIETARY INTERVENTION TRIAL IN MEN WITH PROSTATE CANCER

William J Aronson*, Los Angeles, CA; Stephen J Freedland, Baltimore, MD; Francisco Conde, Naoko Kobayashi, Pinchas Cohen, Tung Ngo, Pak Leung, Susan Bowerman, Jenny Hong, Brandon Varr, Patricia deMiranda, David Elashoff, John Glaspy, Susanne Henning, David Heber, R James Barnard, Los Angeles, CA. Abstract

This page reported by J. Strax, last updated May 18, 2005

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