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Amebic Hepatitis is more prevalent in the tropics but is also found in temperate areas as well.

Obesity-induced insulin resistance and hepatic steatosis are alleviated by {omega}-3 fatty acids: a role for resolvins and protectins. González-Périz A, Horrillo R, Ferré N, Gronert K, Dong B, Morán-Salvador E, Titos E, Martínez-Clemente M, López-Parra M, Arroyo V, Clària J. FASEB J. 2009 Feb 23. [Epub ahead of print] PMID: 19211925 doi: 10.1096/fj.08-125674

Coconut kernel protein modifies the effect of coconut oil on serum lipids. Padmakumaran Nair KG, Rajamohan T, Kurup PA. Plant Foods Hum Nutr. 1999;53(2):133-44. PMID: 10472790 DOI: 10.1023/A:1008078103299 Feeding coconut kernel along with coconut oil in human volunteers has been found to reduce serum total and LDL cholesterol when compared to feeding coconut oil alone. This effect of the kernel was also observed in rats. Since many plant proteins have been reported to exert a cholesterol lowering effect, a study was carried out on the effect of isolated kernel protein in rats. Feeding kernel protein resulted in lower levels of cholesterol, phospholipids and triglycerides in the serum and most tissues when compared to casein fed animals. Rats fed kernel protein had (1) increased hepatic degradation of cholesterol to bile acids, (2) increased hepatic cholesterol biosynthesis, and (3) decreased esterification of free cholesterol. In the intestine, however, cholesterogenesis was decreased. The kernel protein also caused decreased lipogenesis in the liver and intestine. This beneficial effect of the kernel protein is attributed to its very low lysine/arginine ratio 2.13% lysine and 24.5% arginine....

Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins. Kong W, Wei J, Abidi P, Lin M, Inaba S, Li C, Wang Y, Wang Z, Si S, Pan H, Wang S, Wu J, Wang Y, Li Z, Liu J, Jiang JD. Nat Med. 2004 Dec;10(12):1344-51. Epub 2004 Nov 7. PMID: 15531889 doi:10.1038/nm1135 We identify berberine (BBR), a compound isolated from a Chinese herb, as a new cholesterol-lowering drug. Oral administration of BBR in 32 hypercholesterolemic patients for 3 months reduced serum cholesterol by 29%, triglycerides by 35% and LDL-cholesterol by 25%. Treatment of hyperlipidemic hamsters with BBR reduced serum cholesterol by 40% and LDL-cholesterol by 42%, with a 3.5-fold increase in hepatic LDLR mRNA and a 2.6-fold increase in hepatic LDLR protein. Using human hepatoma cells, we show that BBR upregulates LDLR expression independent of sterol regulatory element binding proteins, but dependent on ERK activation. BBR elevates LDLR expression through a post-transcriptional mechanism that stabilizes the mRNA. Using a heterologous system with luciferase as a reporter, we further identify the 5' proximal section of the LDLR mRNA 3' untranslated region responsible for the regulatory effect of BBR. These findings show BBR as a new hypolipidemic drug with a mechanism of action different from that of statin drugs.

CONCLUSIONS: Supplementation with n-3 PUFA improves biochemical, ultrasonographic and haemodynamic features of liver steatosis. Our study supports the efficacy of n-3 PUFA as a new therapeutic approach in the treatment of NAFLD. Prolonged n-3 polyunsaturated fatty acid supplementation ameliorates hepatic steatosis in patients with non-alcoholic fatty liver disease: a pilot study. Capanni M, Calella F, Biagini MR, Genise S, Raimondi L, Bedogni G, Svegliati-Baroni G, Sofi F, Milani S, Abbate R, Surrenti C, Casini A. Aliment Pharmacol Ther. 2006 Apr 15;23(8):1143-51. PMID: 16611275 DOI: 10.1111/j.1365-2036.2006.02885.x

Progression of diethylnitrosamine-induced hepatic carcinogenesis in carnitine-depleted rats. Al-Rejaie SS, Aleisa AM, Al-Yahya AA, Bakheet SA, Alsheikh A, Fatani AG, Al-Shabanah OA, Sayed-Ahmed MM. World J Gastroenterol. 2009 Mar 21;15(11):1373-80. PMID: 19294768

Evaluation of active hexose correlated compound hepatic metabolism and potential for drug interactions with chemotherapy agents. Mach CM, Fugii H, Wakame K, Smith J. J Soc Integr Oncol. 2008 Summer;6(3):105-9. PMID: 19087767

Low vitamin D serum level is related to severe fibrosis and low responsiveness to IFN-based therapy in genotype 1 chronic hepatitis C Salvatore Petta et al. Hepatology, Volume 9999 Issue 999A, Page NA. Published Online: 4 Dec 2009 DOI: 10.1002/hep.23489 Conclusions: G1 CHC patients had low 25(OH)D serum levels, possibly due to reduced CYP27A1 expression. Low vitamin D is linked to severe fibrosis and low SVR on IFN-based therapy. (HEPATOLOGY 2010.)

Vitamin D in preventive medicine: are we ignoring the evidence? Zittermann A. Br J Nutr. 2003 May;89(5):552-72. Review. PMID: 12720576 Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d.

It is not difficult to raise HDLs. This is observed at TYP and in clinical practice ALL THE TIME. Eliminating wheat/d*mn-dirty-GRAINS/carbs, adding some vitamin D, omega-3s, Taurine, and Slo-Niacin 1-2 grams/day. Throwing away the Mazola and any packaged food items. Oh yeah, and add some fat. Individuals may continue their EVO (but not too much b/c it cranks up hepatic lipase, see HERE) but they increase eggs 2-6 daily, add some (organic nitrate-free preferably) bacon and some coconut oil.

Authors of the study reported that carnitine deficiency is a risk factor and should be viewed as a mechanism in hepatic carcinogenesis, and that long-term L-carnitine supplementation prevents the development of liver cancer. Therefore, carnitine supplementation alone or in combination with other natural chemopreventive compounds could be used to prevent, slow or reverse the occurrence of liver cance

Evidence for alteration of the vitamin D-endocrine system in obese subjects. Bell NH, Epstein S, Greene A, Shary J, Oexmann MJ, Shaw S. J Clin Invest. 1985 Jul;76(1):370-3. PMID: 2991340 The results provide evidence that alteration of the vitamin D-endocrine system in obese subjects is characterized by secondary hyperparathyroidism which is associated with enhanced renal tubular reabsorption of calcium and increased circulating 1,25(OH)2D. The reduction of serum 25-OHD in them is attributed to feedback inhibition of hepatic synthesis of the precursor by the increased serum 1,25(OH)2D.

The hypoglycemic effect of fat and protein is not attenuated by insulin resistance. Lan-Pidhainy X, Wolever TM. Am J Clin Nutr. 2009 Nov 18. [Epub ahead of print] PMID: 19923374 doi:10.3945/ajcn.2009.28125 Conclusions: The hypoglycemic effect of fat and protein was not blunted by insulin resistance. Protein increased insulin but had no effect on C-peptide or the insulin secretion rate, which suggests decreased hepatic insulin extraction or increased C-peptide clearance.

"Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides. In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease. Why? Carbohydrates increase small LDL via a multistep process: First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL) Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL. Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL"

Giving saturated fat another chance. Saturated fat has long held a bad rep and been noted for its potential to contribute to cardiovascular disease. So you might understand why I was a bit skeptical of all the hype surrounding the supposedly miracle-working power of coconut oil, which is composed of saturated fatty acids. However, if there's one thing I have learned as a nutrition student, it is that research has the potential to change our views as we continue to expand our knowledge and make new discoveries. Coconut oil may prevent and alleviate disease. Both research and clinical studies have shown that MCFA may be useful in treating and preventing diseases such as diabetes, osteoporosis, virus-related dieases (mononucleosis, hepatitis C, herpes, etc.), gallbladder disease, Crohn's disease, and cancer. The smaller size of MCFA (compared to LCFA) allows them to be digested more easily, making them ideal for those suffering from digestive diseases. Coconut oil may assist in the absorption and retaining of calcium, thereby benefiting bones. Coconut oil has antimicrobial, antiviral, and antifungal properties. Lipid-coated bacteria and viruses contain a lipid coat which encloses their DNA among other cellular materials. When consumed by humans, coconut oil disrupts the lipid membrane, killing the pathogens without damaging the host or harming health-promoting intestinal bacteria. The antimicrobial properties stem from the monoglycerides and free fatty acids (mainly lauric acid and capric acid) that compose coconut oil.

(NaturalNews) In a time when strange viruses are making headlines around the world, perhaps it's time you knew about the most powerful natural antiviral around: coconut oil. The antiviral activity in coconut oil is unparalleled, even among the most resistant viruses, and the best part is, if it's virgin and organic, there isn't a man-made chemical in the mix. Think it's too good to be true? Bruce Fife, C.N., N.D. and author of The Coconut Oil Miracle shares, "Laboratory tests have shown that the MCFAs (medium chain fatty acids) found in coconut oil are effective in destroying viruses that cause influenza, measles, herpes, mononucleosis hepatitis C, and AIDS; bacteria that can cause stomach ulcers, throat infections, pneumonia, sinusitis, urinary tract infections, meningitis, gonorrhea, and toxic shock syndrome; fungi and yeast that lead to ringworm, candida, and thrush; and parasites that can cause intestinal infections such as giardiasis." Sounds like a powerhouse to me.

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. J Clin Invest. 2009 May;119(5):1322-34. Epub 2009 Apr 20. PMID: 19381015 doi: 10.1172/JCI37385. Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

"5' AMP-activated protein kinase or AMPK or 5' adenosine monophosphate-activated protein kinase is an enzyme that plays a role in cellular energy homeostasis. It consists of three proteins (subunits) that together make a functional enzyme, conserved from yeast to humans. It is expressed in a number of tissues, including the liver, brain, and skeletal muscle. The net effect of AMPK activation is stimulation of hepatic fatty acid oxidation and ketogenesis, inhibition of cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibition of adipocyte lipolysis and lipogenesis, stimulation of skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulation of insulin secretion by pancreatic beta-cells.[1] It should not be confused with cyclic AMP-activated protein kinase (protein kinase A), which, although being of similar nature, may have opposite effects.[2]"

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ScienceDaily (Feb. 12, 2009) - According to a recent study, diets rich in omega-3 fatty acids protect the liver from damage caused by obesity and the insulin resistance it provokes. This research should give doctors and nutritionists valuable information when recommending and formulating weight-loss diets and help explain why some obese patients are more likely to suffer some complications associated with obesity. Omega-3 fatty acids can be found in canola oil and fish.