Научная статья на тему 'Nutraceuticals and wild foods and risk of cardiovascular disease'

Nutraceuticals and wild foods and risk of cardiovascular disease Текст научной статьи по специальности «Биотехнологии в медицине»

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Текст научной работы на тему «Nutraceuticals and wild foods and risk of cardiovascular disease»

NUTRACEUTICALS AND WILD FOODS AND RISK OF CARDIOVASCULAR DISEASE.

R B Singh, RS Tomar, RK Singh; Chibiso Sergey M. Radzhesh Agarwal, Fabien De Meester, Agnieszka Wilczynska-Kwiatek;Halberg Hospital and Research Institute, Moradabad, NCRG, Junagarh, Mukteswar,India; Department of Patho-Physiology, People,s Friendship University of Russia; Tsim Tsoum Institute, Krakow, Poland.

Correspondence:Prof.Dr RB Singh,MD Director, Halberg Hospital and Research Institute Civil Lines, Moradabad-10(UP) 244001, India email icn2005@sancharnet.in tel 0591 2417437

The seven country study showed that the mortality due to coronary artery disease was continuous and graded with rise in serum cholesterol. However, there was variation in mortality rates in different countries at the same levels of serum cholesterol. It is possible that antioxidants; flavonoids, vitamins A,E,C , minerals; copper, zinc, selenium and chromium and w-3 fatty acids present in the diet may explain, the cause of the variation in risk of coronary artery disease and cancer mortality in various countries. Indian diets are rich in antioxidant vitamins A,E,C and betacarotine and various flavonoids and the consumption of fruits,vegatables and legumes varies between 50-500g/day,( average 200g/day),according to five city study. The main sources of antioxidants in the diets are fruits, vegetables, oils, sprouted seeds, and herbs. In Kerala, coco nuts are rich sources of tocoferols and tocotrenols and fish is rich in selenium and coenzyme Q10.If we consider, only these two foods to assess antioxidant in the diets, the contents appear to be enough to prevent cardiovascular disease. Fish is a rich source of w-3 fatty acids and coenzyme Q10.

These agents present in the foods may be called nutraceuticals because they are now available in the market as therapeutic agents. The content and concentration of particular nutrients can be altered by feeding nutrient rich feeds to animals and by enhancing the nutrients in the soil which is a feed for plants. Genetic engineering and plant breeding may be also used to enhance the nutrient content of plant foods. While Dr Sim from Canada has increased the w-3 fatty acid content of hen,s eggs, by feeding flax seeds, Kang has developed w-3 fatty acid rich mice by genetic manipulations (Nature 2002). Magnesium, potassium, sodium and calcium present in the foods can influence AT-pases and related ion channels present in cell membranes. Coenzyme Q10 and carnitine are rich in muscles including cardiac muscles and can be enhanced by regular physical activity and therapeutic supplementation. We have been using several of these nutrients and nutraceuticals for treatment of CVD and diabetes in clinical practice.

Recent studies indicate that free radicals, nitric oxide(NO), eicosanoids, pro and anti-inflammatory cytokines, long chain polyunsaturated fatty acids, folic acid, tetrahydrobiopterin(BH4) and vitamin C play a significant role in the pathogenesis of cardiovascular disease. These molecules can interact with angiotensin converting enzyme (ACE), endothelins, antihypertensive drugs such as calcium channel blockers, beta-blockers and ACE-inhibitors indicating their role in the prevention of CVD. Troglitazone down regulates delta-6 desaturase gene expression in human skeletal muscle cell cultures, associated with a change in the unsaturated fatty acid composition of the muscle cells. Dexamethasone induced reductions in the piglet arachidonic acid status is minimized by dietary w-3 supplement. Piglets treated with dexamethasone grew slower and had lower bone mineral content of whole body and lower levels of arachidonic acid.

Oxidative modification of LDL enhances the atherogenesity of cholesterol and enhances the development of atherosclerosis and thrombosis whereas dietary antioxidants and w-3, prevent oxidation of LDL, and therefore, coronary artery disease(CAD), type 2 diabetes and hypertension associated vascular disease. While foods rich in micronutrients have been observed to be protective, large therapeutic doses of vitamin E, and betacarotine, folic acid, vitamin B6, as supplement showed no effects or adverse effects in several studies. In a recent study, vitamin E and C decreased the lipid lowering efficacy of niacin and statins by 50%.Vitamin E supplementation in higher doses>100mg/day may also reduce gama tocoferol as well as HDL-cholesterol which have adverse effects.

Application of molecular biology techniques indicated that PUFA elicit changes in gene expression that precede changes in membrane composition by directly governing the activity of nuclear transcription factors . PUFA regulation of gene transcription occurred within a matter of minutes: such a time frame was too rapid to be explained simply by changes in membrane composition and altered hormone release or signaling, but is most consistent with a ligand mediated event . Recent research indicate novel perspectives for deeper understanding of energy metabolism and therapeutic interventions. Peroxisome proliferater -activated receptor-a[PPAR- a]was the first transcription factor identified as a prospective fatty acid receptor. PPAR- a plays a role in the regulation of an extensive network of genes involved in glucose and lipid metabolism. In animal models, w-6 and w-3 fatty acids are potent inducers of fatty acid oxidation and potent suppressors of fatty acid and triacylglycerol synthesis . It is clear that PUFA are potent PPAR activators.

Experimental studies revealed that, in animals fed with a diet rich in 20-carbon and 22-carbon PUFA, the expression of the genes may be associated with high rates of fat oxidation and reduced body fat deposition . It has been established that the 5 ’flanking regions of genes encoding carnitine palmitoytransferase , acyl-CoA oxidase, mitochondrial hydroxymethylglutaryl-CoA synthase , fatty acyl-CoA synthetase and mitochondrial uncoupling proteins all contain DNA recognition sequences for PPAR. However, studies with the PPAR- a null mouse have shown that PPAR- a is not the sole transcription factor involved in mediating fatty acid effects on gene transcription.

Desvergne and Wahli, reported that activated PPAR-y induces lipoprotein lipase and fatty acid transporters and enhances adipocyte differentiation as well as inhibits the function of the transcription factor NF-kB and cytokines, and therefore COX-2 expression . PPAR- y also binds 20:5 n-3. In experimental studies, drug induced activation of PPAR- a and PPAR-y, reduces lipid levels in muscle and adipose tissue and improves insulin sensitivity . Omega-3 PUFA are weak

Материалы X международного конгресса «Здоровье и образование в XXI веке» РУДН, Москва

agonists of PPAR as compared with drug agonists (e.g. thiazolidinediones ), these fatty acids have significant effects on insulin sensitivity in various tissues , particularly skeletal muscle .

In addition to the PPAR family (PPAR- a, p, -y1, and -y2) several other transcriiption factors have been indentified as targets for fatty acid regulation, including hepatic nuclear factor-4a (HNF- 4a), sterol regulatory element-binding protein (SREBP), liver X receptors (LXR- a and -P), retinoid X receptors (RXR-a) , and NF-kB . It is note worthy to mention that in order to bind to DNA and activate transcription, PPAR required the formation of heterodimers with RXR. Recently, the liver X receptors (LXR- a and LXR-P ) were identified as targets for fatty acid regulation . LXRs bind oxysterols and regulate the expression of genes involved in hepatic bile acid synthesis .PUFA antagonize oxysterol activation by LXR- a in HEX 293 and hepatoma cell lines by interfering with oxysterol binding.

The US preventive service task force and the International College of Nutrition recommends against the use of beta-carotine and large doses of vitamin E, folic acid and B6, for prevention of cardiovascular disease till further evidence.Since oxidative stress continue to be important in the modification of LDL,myocardial damage and endothelial dysfunction, therefore,people should obtain their antioxidants from wild foods which are grown in a natural environment in a soil rich in useful nutrients. The International College Of Cardiology, World Council of Body and Mind and International College of Nutrition advise that eating 400g/day of Fruits,vegetable,nuts and another 400g/day of whole grains +30-50g/day of mustered oil which can provide desired amount of micronutrients for prevention of CVD and diabetes and cancer. This advise is based on the findings of the Lyon Heart Study( Renaud group, Lancet 2004,France), the Indo-Mediterranean Diet-Heart Study (Singh et al, Lancet 2002,India) and The Diet and Re-infarction Trial( Burr et al, 1999,UK) and several long term follow-up studies.

ЛИТЕРАТУРА

1. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2011г.

2. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2010г.

3. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2009г.

4. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2008г.

5. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2007г.

6. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2006г.

7. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2005г.

8. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2004г.

9. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2003г.

10. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2002г.

11. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2001г.

12. Сборник научных тезисов и статей «Здоровье и образование в XXI веке», Москва, 2000г.

13. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2011г.

14. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2010г.

15. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2009г.

16. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2008г.

17. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2007г.

18. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2006г.

19. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2005г.

20. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2004г.

21. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2003г.

22. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2002г.

23. Электронный сборник научных трудов «Здоровье и образование в XXI веке». 2001г.

Материалы! X международного конгресса «Здоровье и образование в XXI веке» РУДН, Москва

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