Eine westliche Ernährungsweise (Diät) mit einem hohen Anteil an Kohlenhydraten und mehr Omega-6 (mehrfach ungesättigten pflanzlichen) Fetten führt in den folgenden Generation zu mehr Fettleibigkeit, auch wenn man die Ernährung wieder umstellt!

Was ich wissen muss:

Weniger Omega-6 Fettreiche Nahrung konsumieren wie z.B:

• Margarine
• Pflanzliche Keim-Öle wie:
  • Maiskeimöl
  • Rapsöl
  • Sojaöl (=Speiseöl)
• Alle Produkte mit „teilweise gehärteten Pflanzenfetten“

Ersetzen durch:

• Gras-gefütterte Bio-Butter
  • Gras sorgt für mehr Omega-3
• Kaltgepresstes natives Olivenöl
  • Nicht zum Braten; Mehr einfach ungesättigte Fette und damit weniger Omega-6
• Bio-Schmalz
  • Sehr ähnlich dem Olivenöl, jedoch durch die gesättigen Fette auch Hitzestabil
• Nativ gepresstes Kokosnuss Öl
  • Nicht Kokusfett aus dem Kühlregal – dieses ist tlw. gehärtet!
• Sparsam: Spezielles Brat-Öl mit dem Zusatz „High Oleic“
  • Viel Ölsäure – oft aus Sonnenblumenkernen gewonnen
• Fisch-Öl (z.b: Lebertran) als Nahrungsergänzungsmittel für mehr Omega-3

Dies ist eine französische Studie an Mäusen aus dem Jahr 2010. Die Forscher haben hierzu Mäuse in zwei Gruppen eingeteilt. Eine Gruppe hat eine standard Labor Ernährung (Chow -43,6% Kohlehydrate – 35% Fett – 21,4% Eiweiss) bekommen, die andere Gruppe hat eine Diät mit der gleichen Aufteilung, jedoch einem 3,7x höheren Anteil Omega-6 Fett (pflanzliches Fett wie man es z.B. in Maiskeimöl oder Margarine findet) gegessen.

Die Mäuse wurden dann zufällig gepaart und in folgenden Generation auch weiter in diese Gruppen aufgeteilt.

Wie die Wissenschafler schreiben: Kombiniert mit hohem Kohlenhydrat Inhalt, ist die Omega-6 reiche Ernährungsweise pro-fettbildend.

Gesamt gesehen unterstreichen diese Ergebnisse das die Bildung von Fettgewebe neben [viel] Fett in der Ernährung vor allem in Kombination mit [Hervorhebung durch die Forscher] einem hohen Omega-6 zu Omega-3 Verhältnis zusammenhängt.

When combined with high carbohydrate content, a linoleic acid-enriched diet was found to be pro-adipogenic […]

Overall, these results emphasize the importance of adipose tissue development in rodents of a high-fat diet combined with a high LA:LNA ratio

Ich denke das diese Schlussfolgerung etwas irreführend ist. Schließlich haben beide Gruppen DIE GLEICHE Menge Fett bekommen. Es hängt also nicht direkt mit dem Fett, als vielmehr mit der Fettzusammensetzung zusammen. Auch merken die Forscher an, das der Beitrag von Fetten aus der Nahrung in Kombination mit einer höheren Energiezufur sehr kontrovers sind, da in den letzten zwei Jahrzenten bei der Bevölkerung keine Erhöhung der Fettmenge festgestellt wurde (sehr wohl aber eine Zunahme an Übergewichtigen).

However, the contribution of dietary fats compared with an excess energy intake in increasing body weight remains controversial, as no major change in the total amount of ingested fats has occurred in the last two decades

Neben dem reinen Kalorien zählen, ist die Qualitätsfrage in letzter Zeit als Risikofaktor in den Vordergrund gerückt. Das Ungleichgewicht zwischen Omega-6 und Omega-3 (beides mehrfach ungesättigte Fettsäuren) scheint ein wichtiger Faktor zu sein.

In addition to caloric excess, a qualitative issue has emerged as a risk factor for obesity in rodents and possibly in humans; i.e., the disequilibrium in polyunsaturated fatty acid (PUFA) metabolism with a high ratio of linoleic acid (C18:2 ω6, LA) versus α-linolenic acid (C18:3 ω3, LNA)

Besonders hervorzuheben ist, das bei Nagern eine Reduzierung von 59:1 auf 2:1 (Omega-6:Omega-3) unter gleichbleibenden Kalorien UND Fett-Anteilen der Nahrung diesen (Körper-fettbildende) Bedingungen entgegengewirkt werden kann.

Notably, in rodents, reducing this ratio from 59 to 2 under isolipidic, isoenergetic conditions (40% energy as fat) by inclusion of dietary LNA counteracted the enhancing effects […].

 

A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations
Florence Massiera, Pascal Barbry, Philippe Guesnet, Aurélie Joly, Serge Luquet, Chimène Moreilhon-Brest, Tala Mohsen-Kanson, Ez-Zoubir Amri, and Gérard Ailhaud

Noch einige weitere Zitate aus der Studie im englischen Original:

For this purpose, male and female mice were chronically exposed over four generations to a single Western-like fat diet; i.e., 35% energy as fat with a of [Omega-6 Fatty Acid] LA/[Omega-3 Fatty Acid] LNA ratio similar to that found in the most consumed foods.

 

The results show that this condition was sufficient to trigger gradual transgenerational enhancement of the fat mass observed at early and adult ages.

 

The [Omega-6 Western Diet] ω6HFD contained a 3.7-fold higher amount of [Omega-6 Fatty Acid] LA (7.9 g per 100 g versus 2.2 g per 100 g) but the same amount of [Omega-3 Fatty Acid] LNA.

 

HF0–HF4 [Western Diet offspring] mice were continuously exposed over generations to the isocaloric, isolipidic diet […].

 

However, when the adult male and female HF0 [Western Diet offspring] mice on the [Omega-6 Western Diet] ω6HFD were mated randomly and produced HF1 pups, the body weight of the male mice at weaning became significantly higher […].

 

Regarding fat mass, a large difference in the weight of the epididymal fat pad was already observed across generations at 8 weeks for [Western Diet offspring] HF0, HF1, and HF2 mice[…].

 

This finding showed that the [Omega-6 Western Diet] ω6HFD  had no impact upon reproduction, thus excluding the possibility that litter size could explain an indirect effect of the diet across generations[…].

 

Moreover, when [Western Diet offspring] HF4 pups were transferred at weaning to a chow diet the food intake of revHF4 mice (n = 3) remained similar to that of HF4 and previous generations. Thus, these results exclude the possibility that changes in food and fat intake—across generations early and late in life—explain the transgenerational increase in body weight and fat mass observed at the adult age, suggesting that other mechanisms are implicated.

 

PUFA [i.e. Omega-6 and Omega-3 Fatty Acids] metabolism in the mothers‘ milk lipids was altered in response to the linoleic acid-enriched diet but then remained similar across generations.

 

In contrast, it decreased significantly the content of long-chain polyunsaturated fatty acids (LC-PUFA) of the ω3 series, i.e., eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), All these observations are in agreement with human studies showing that an increase in [Omega-6 Fatty Acid] LA intake leads to stimulation of ARA and/or inhibition of EPA and DHA synthesis[…].

 

The ARA:EPA+DHA ratio increased more than 2-fold in [Western Diet offspring] HF4 mice and reversed completely in [Western Diet offspring, eating normal chow] revHF4 mice. A reversible pattern was also observed for the ω6 and ω3 PUFA composition of adipose tissue lipids. Under these conditions, the body weight of revHF4 mice returned 5 weeks later to that of HF0 mice. Importantly, a similar but incomplete reversal was observed for the epididymal fatpad weight […].

 

The incomplete reversal of the adipose phenotype at later generations suggested that some transgenerational memory had been acquired, allowing revHF4 mice to respond more rapidly than STD mice to the [Omega-6 Western Diet] ω6HFD […].

 

Those fed the [Omega-6 Western Diet] ω6HFD for 19 weeks after weaning exhibited an increase in the plasma level of most parameters traditionally associated with the metabolic syndrome (i.e., TNFα, resistin, insulin, leptin, and MCP-1) in the first, second, and third generationFasting insulin levels followed a pattern similar to that of cytokines but remained significantly higher than those of HF0 mice. These observations indicate that, despite the fact that glycemia in HF4 mice appeared normal at 22 weeks old (151 ± 30 mg/dl for HF4 versus 170 ± 30 mg/dl for STD mice), continuous exposure to the [Omega-6 Western Diet] ω6HFD  led to a sustained increase in plasma insulin levels, which strongly suggests the emergence of insulin resistance of adult animals at later generations.

 

Notably, at a time where overweightness and obesity have steadily increased over generations in most industrialized countries, consumption of [Omega-6 Fatty Acid] LA and ARA has increased. In France, an increase of 250% and 230%, respectively, occurred from 1960 to 2000 . During the same period, consumption of [Omega-3 Fatty Acid] LNA has decreased by 40%, resulting in a 4.2-fold increase in the LA:[Omega-3 Fatty Acid] LNA ratio. A similar increase in [Omega-6 Fatty Acid] LA intake has been observed in other countries of the Western world, with a LA:[Omega-3 Fatty Acid] LNA ratio ranging from 10 to 41 for most foods consumed in the US. Under isolipidic, isoenergetic [same fat composition, same amount of calories] conditions, an [Omega-6] LA-enriched diet was shown in elderly humans to increase body weight, and the rate of [Omega-6 Fatty Acid] LA accumulation in adipose tissue was associated positively with gain in body weight.

 

Noteworthy, enhanced adiposity occurs over generations through hyperplasia and hypertrophy despite no significant change in food intake in pups and adult mice[…].

 

The most persistent dysregulation was that of insulin. In the absence of hyperglycemia, this strongly suggests insulin resistance, which is consistent with a progressive loss in sympathetic inhibition of insulin release over generations. Thus it looks as if an enhanced fat mass was an adaptive response to prevent aggravation of a metabolic syndrome.

 

Collectively, our data show that continuous exposure to a high-fat diet combined with a high LA:[Omega-3 Fatty Acid] LNA ratio from fetal to adult age over generations triggers a discrete and steady increase in inflammatory stimuli accompanied by enhancement of fat mass that was already observed a few weeks after birth. Most interestingly, in humans, the recent Framingham Heart study pointed out that nonobese offspring with two obese parents had higher C-reactive protein levels compared with offspring with one or no obese parent. Thus offspring with a high risk of developing obesity are characterized at birth by a proinflammatory state.