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Preformed DHA from Algae Oil Could Help Bypass Liver Metabolism Defect

 

 

Defect in Liver Metabolism Could Cause DHA Deficiency in Alzheimer's

Researchers have discovered that markedly depleted amounts of an omega-3 fatty acid in brain tissue samples from Alzheimer's patients may be due to the liver's inability to produce the complex fat, also contained in fish-oil supplements.

Low levels of docosahexaenoic acid, or DHA, have been associated with the chronic neurodegenerative disease affecting millions of Americans, but no cause had been identified.

In postmortem liver tissue from Alzheimer's patients, the team found a defect in the organ's ability to make DHA from shorter molecules present in leafy plants and other foods. Previous studies have shown that most brain DHA is manufactured in the liver.

Non-Alzheimer's livers did not have this defect, said Daniele Piomelli, who led the research with Giuseppe Astarita.

"We all know Alzheimer's is a brain disease, but our findings – which were totally unexpected – show that a problem with liver fat metabolism can make people more vulnerable," Piomelli said. "They also suggest a reason why clinical trials in which Alzheimer's patients are given omega-3 fatty acids to improve cognitive skills have had mixed results."

DHA occurs naturally in cold-water fatty fish and seaweed. It is essential for the proper functioning of adult human brains and for the development of our nervous system and vision during the first six months of life. Omega-3 fatty acids are also part of a healthy diet that helps lower risk of heart disease.

"Additionally, we found that the greater the amount of Alzheimer's-related cognitive problems experienced in life by the patients, the lower were their liver DHA levels," Astarita said. "So we do see a connection."

Piomelli added that the results point to new diagnostic and dietary approaches to Alzheimer's: Specific blood lipid profile tests might identify at-risk persons, and dietary supplements with a chemically enhanced form of DHA may benefit early-stage patients.

"Our research isn't advocating that liver metabolism is a key to Alzheimer's," he noted. "The factors causing the disease are many and complex, but we feel this is another piece in the Alzheimer's puzzle."
 
References:
1. Giuseppe Astarita, et al. Deficient Liver Biosynthesis of Docosahexaenoic Acid Correlates with Cognitive Impairment in Alzheimer's Disease. PLoS ONE, 2010; 5 (9): e12538 DOI: 10.1371/journal.pone.0012538

Microalgae oil superfood is not seaweed, but same Chromista kingdom; DHA to help Alzheimer's

Liver defect likely cause of DHA deficiency in Alzheimer’s patients, UCI study finds

http://today.uci.edu/news/2010/09/nr_dha_100908.php

Low levels of the omega-3 fatty acid may contribute to the neurodegenerative disease

— Irvine, Calif., September 08, 2010 —

UC Irvine researchers have discovered that markedly depleted amounts of an omega-3 fatty acid in brain tissue samples from Alzheimer’s patients may be due to the liver’s inability to produce the complex fat, also contained in fish-oil supplements.

Low levels of docosahexaenoic acid, or DHA, have been associated with the chronic neurodegenerative disease affecting millions of Americans, but no cause had been identified.

In postmortem liver tissue from Alzheimer’s patients, the UCI team found a defect in the organ’s ability to make DHA from shorter molecules present in leafy plants and other foods. Previous studies have shown that most brain DHA is manufactured in the liver.

Non-Alzheimer’s livers did not have this defect, said Daniele Piomelli, the Louise Turner Arnold Chair in the Neurosciences and director of the Center for Drug Discovery at UCI, who led the research with Giuseppe Astarita, project scientist in pharmacology.

“We all know Alzheimer’s is a brain disease, but our findings – which were totally unexpected – show that a problem with liver fat metabolism can make people more vulnerable,” Piomelli said. “They also suggest a reason why clinical trials in which Alzheimer’s patients are given omega-3 fatty acids to improve cognitive skills have had mixed results.”

The study appears Sept. 8 in the open-access, peer-reviewed journal PLoS ONE.

DHA occurs naturally in cold-water fatty fish and seaweed. It is essential for the proper functioning of adult human brains and for the development of our nervous system and vision during the first six months of life. Omega-3 fatty acids are also part of a healthy diet that helps lower risk of heart disease.

“Additionally, we found that the greater the amount of Alzheimer’s-related cognitive problems experienced in life by the patients, the lower were their liver DHA levels,” Astarita said. “So we do see a connection.”

Piomelli added that the results point to new diagnostic and dietary approaches to Alzheimer’s: Specific blood lipid profile tests might identify at-risk persons, and dietary supplements with a chemically enhanced form of DHA may benefit early-stage patients.

“Our research isn’t advocating that liver metabolism is a key to Alzheimer’s,” he noted. “The factors causing the disease are many and complex, but we feel this is another piece in the Alzheimer’s puzzle.”

Carl Cotman, Kwang-Mook Jung, Nicole C. Berchtold, Vinh Q. Nguyen and Daniel L. Gillen of UCI’s Institute for Memory Impairments and Neurological Disorders contributed to the study, along with Elizabeth Head of the University of Kentucky’s Sanders-Brown Center on Aging.

About the University of California, Irvine: Founded in 1965, UCI is a top-ranked university dedicated to research, scholarship and community service. Led by Chancellor Michael Drake since 2005, UCI is among the most dynamic campuses in the University of California system, with nearly 28,000 undergraduate and graduate students, 1,100 faculty and 9,000 staff. Orange County’s largest employer, UCI contributes an annual economic impact of $3.9 billion. For more UCI news, visit www.today.uci.edu.

News Radio: UCI maintains on campus an ISDN line for conducting interviews with its faculty and experts. Use of this line is available for a fee to radio news programs/stations that wish to interview UCI faculty and experts. Use of the ISDN line is subject to availability and approval by the university.

DR DHA SAYS: DHA-rich microalgae oil will do the trick for both

Question by George Bernard Shaw: Cholesterol, Triglycerides, HDL, LDL, exercise?
http://lower-my-cholesterol.net/35001/qa-cholesterol-triglycerides-hdl-ldl-exercise-2/

www.source-omega.com

I had a fasting blood test show the following results:
CHOLESTEROL 108 MG/DL
TRIGLYCERIDES 204 MG/DL
HDL 21 MG/DL
LDL 46 MG/DL

I was flagged as high on the triglycerides and low on the HDL. I eat a very healthy diet including baked chicken, no red meat, and greens, and drink nothing but skim milk or water. Occasionally I have some cranberry juice. I don’t smoke, drink alcohol or caffeine. I need to start getting some exercise, but my question is… Will exercise drop my triglycerides and raise my HDL levels alone..or do I need to eat certain foods? I don’t eat egg yolks.

 

DR DHA SAYS: DHA-rich microalgae oil will do the trick for both.

Algae oil GMP status, quality and purity unmatched for long chain omega-3s

Dietary Supplement Briefing Held on Capitol Hill

 

Published September 9, 2010
 
The Congressional Dietary Supplement Caucus (DSC), in cooperation with two trade associations representing the dietary supplement industry—the Natural Products Association (NPA) and the Council for Responsible Nutrition (CRN)—held a briefing on Capitol Hill yesterday to debunk some of the untruths and misconceptions about the dietary supplement industry and its role in Americans’ wellness regimens.
 
“It’s all about prevention. Prevention is the new mantra among consumers,” said guest speaker Patrick Rea, publisher and editorial director of Nutrition Business Journal (NBJ). Speaking to an audience of staff members from the U.S. House and Senate, Rea said that even during tough economic times, consumers turn to dietary supplements as an important part of their immunity and prevention plan. “Consumers looked at supplements as one way through the recession to help take care of themselves. Health is recession resilient, and the sales over time support this fact,” said Rea. 
 
Rea cut through some of the misconceptions and rhetoric too frequently reported as fact, and offered a true view of the state of the industry. He directly addressed several of what he called “industry myths” –that dietary supplements are unnecessary because people get what they need from food; that people really do not want to take supplements; that the pharmaceutical industry will destroy the dietary supplement industry; and that the industry is unregulated.
 
Rea shared solid sales and product trend data that refuted each myth, and explained in depth how an aging but influential population is changing the way Americans use and rely on dietary supplements. Dietary supplements are part of a nearly $27 billion industry that has demonstrated steady sales and product growth over time. “Our numbers show that somewhere between 60-80 percent of Americans take supplements, and 48 percent of them consider themselves regular users,” said Rea. 
 
Rea also mentioned the growing acceptance of dietary supplements among conventional health practitioners, and the growing trend among pharmaceutical companies to develop their own versions of products usually sold as supplements. “In a study of healthcare professionals, 72 percent of physicians and 89 percent of nurses are dietary supplement consumers, and of that group, 79 percent of physicians and 82 percent of nurses recommend dietary supplements to their patients,” said Rea.
 
Rea concluded by disputing the myth that the industry is unregulated. “The supplement industry is one of the more highly regulated industries. Many of the companies say the regulatory challenges they face today are the threat of increased FDA and FTC regulation over the industry, and the recent GMP [good manufacturing practices] rollout. A lot of the companies are rallying behind the GMP regulations. They want it to be known that they are a GMP-compliant company. And, the Dietary Supplement Health Education Act [DSHEA] made claims rules clear and has really helped the industry focus and develop,” said Rea.
 
“What is the truth about the dietary supplement industry? There is a lot of investment in science, and a lot of movement by companies to ensure they’re up to speed on the regulatory front,” said Rea.

 

 

Is DHA-Rich Algae Oil good for Zellweger Syndrome?

The delta4-desaturation pathway for DHA biosynthesis is operative in the human species: Differences between normal controls and children with the Zellweger syndrome

click here to read more

Docosahexaenoic acid (DHA, 22:6) is a fundamental component of cell membranes, especially in the brain and retina. In the experimental animal, DHA deficiency leads to suboptimal neurological performance and visual deficiencies.

Children with the Zellweger syndrome (ZS) have a profound DHA deficiency and symptoms that can be attributed to their extremely low DHA levels. These children seem to have a metabolic defect in DHA biosynthesis, which has never been totally elucidated.

Treatment with DHA ethyl ester greatly improves these patients, but if we could normalize their endogenous DHA production we could get additional benefits. We examined whether DHA biosynthesis by Delta4-desaturation could be enhanced in the human species by transfecting the enzyme, and if this could normalize the DHA levels in cells from ZS patients.

Results: We showed that the Delta4-desaturase gene (Fad4) from Thraustochytrium sp, which can be expressed by heterologous transfection in other plant and yeast cells, can also be transfected into human lymphocytes, and that it expresses the enzyme (FAD4, Delta4-desaturase) by producing DHA from direct Delta4-desaturation of 22:53.

We also found that the other substrate for Delta4-desaturase, 22:46, was parallely desaturated to 22:5 6.

Conclusions: The present "in vitro"study demonstrates that Delta4-desaturase can be transfected into human cells and synthesize DHA (as well as 22:56, DPA) from 22:53 and 22:46 respectively, by putative Delta4-desaturation. Even if this pathway may not be the physiological route for DHA biosynthesis "in vivo", the present study opens new perspectives for the treatment of patients within the ZS spectrum.

Author: Manuela MartinezNatalia IchasoFernando SetienNuria DuranyXiao QiuWilliam Roesler
Credits/Source: Lipids in Health and Disease 2010, 9:98

 

Algae oil and G-protein mechanism, is there a link?

GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent Anti-inflammatory and Insulin-Sensitizing Effects

Cell, Volume 142, Issue 5, 687-698, 3 September 2010
Copyright © 2010 Elsevier Inc. All rights reserved.
10.1016/j.cell.2010.07.041

Referred to by: Fishing Out a Sensor for Anti-inflammato...

Authors

  • Highlights
  • GPR120 is expressed in macrophages and Kupffer cells and is induced in obesity
  • GPR120 functions as an omega 3 fatty acid (?-3 FA) receptor/sensor
  • ?-3 FAs exert broad anti-inflammatory effects through GPR120 in macrophages
  • GP120 mediates insulin sensitization by ?-3 FAs in obese mice

Summary

Omega-3 fatty acids (?-3 FAs), DHA and EPA, exert anti-inflammatory effects, but the mechanisms are poorly understood. Here, we show that the G protein-coupled receptor 120 (GPR120) functions as an ?-3 FA receptor/sensor. Stimulation of GPR120 with ?-3 FAs or a chemical agonist causes broad anti-inflammatory effects in monocytic RAW 264.7 cells and in primary intraperitoneal macrophages. All of these effects are abrogated by GPR120 knockdown. Since chronic macrophage-mediated tissue inflammation is a key mechanism for insulin resistance in obesity, we fed obese WT andGPR120 knockout mice a high-fat diet with or without ?-3 FA supplementation. The ?-3 FA treatment inhibited inflammation and enhanced systemic insulin sensitivity in WT mice, but was without effect in GPR120 knockout mice. In conclusion, GPR120 is a functional ?-3 FA receptor/sensor and mediates potent insulin sensitizing and antidiabetic effects in vivo by repressing macrophage-induced tissue inflammation.