But what does the science say? A systematic review and meta-analysis published in the Journal of the American Medical Association,highlighted in my video Is Fish Oil Just Snake Oil? looked at all the best “randomized clinical trials evaluating the effects of omega-3’s on lifespan, cardiac death, sudden death, heart attack, and stroke.” The studies told the subjects to either eat more oily fish or to take fish oil capsules. What did the study find? Overall, the researchers found no protective benefit for all-cause mortality, heart disease mortality, sudden cardiac death, heart attack, or stroke.
What about for those who already had a heart attack and are trying to prevent another? Still no benefit. Where did we even get this idea that omega 3’s were good for the heart? If we look at some of the older studies, the results seemed promising. For example, there was the famous DART trial back in the 80s involving 2,000 men. Those advised to eat fatty fish had a 29% reduction in mortality. Pretty impressive—no wonder it got a lot of attention. But people seemed to have forgotten the sequel, the DART-2 trial. The same group of researchers, and an even bigger study (3,000 men). In DART-2 “those advised to eat oily fish and particularly those supplied with fish oil capsules had a higher risk of cardiac death.”
Put all the studies together, and there’s no justification for the use of omega 3s as a structured intervention in everyday clinical practice or for guidelines supporting more dietary omega-3’s. So what should doctors say when their patients follow the American Heart Association advice to ask them about fish oil supplements? Given this and other negative meta-analyses, “our job as doctors should be to stop highly marketed fish oil supplementation in all of our patients.”
I’ve previously discussed fish oil supplements in the context of risks versus purported cardiovascular benefits:
- Dietary Supplement Snake Oil
- Fish Oil in Troubled Waters
- DDT in Fish Oil Supplements
- Is Cod Liver Oil Good For You?
- Are krill oil supplements better than fish oil capsules?
But if the benefits aren’t there, then all one is left with are concerns over the industrial pollutants that concentrate in the fish fat (even in distilled fish oil, see Is Distilled Fish Oil Toxin-Free?).
- Fish Intake Associated With Brain Shrinkage
- Mercury vs. Omega-3s for Brain Development
- How Long to Detox From Fish Before Pregnancy?
–Michael Greger, M.D.
PS: If you haven’t yet, you can subscribe to my free videos here and watch my live year-in-review presentations Uprooting the Leading Causes of Death, More Than an Apple a Day ,and From Table to Able.
Image Credit: Jo Christian Oterhals / Flickr
I saw this talk in San Francisco and it was one of the most amazing new findings I recently heard of:
At TEDMED 2014, neuroscientist Jeff Iliff illuminates a newly discovered, critical function of the brain during sleep, a natural cleansing system that keeps toxic proteins at bay.
I’d be curious to hear if anyone experiences similar results. Even if the study was just a fluke, Nuts May Help Prevent Death by improving the function of our arteries (Walnuts and Artery Function) and fighting cancer (Which Nut Fights Cancer?) and inflammation (Fighting Inflammation in a Nut Shell).
Even eating nuts every day does not appear to result in expected weight gain (Nuts and Obesity: The Weight of Evidence), so enjoy!
Source: Dr. Greger – nutritionfacts.org
Erectile dysfunction is the recurrent or persistent inability to attain and/or maintain an erection in order for satisfactory sexual performance. It is present in up to 30 million men in the U.S. and approximately 100 million men worldwide. The U.S. has less than 8% of the world’s population, yet up to 30% of the impotence? We’re #1!
But hey, we’ve got red, white, and blue pills like Viagra. The problem is that the pills just cover up the symptoms of vascular disease and don’t do anything for the underlying pathology. Erectile dysfunction and our #1 killer, coronary artery disease, are just two manifestations of the same disease: inflamed, clogged, and crippled arteries, regardless of which organ it affects (See Survival of the Firmest: Erectile Dysfunction and Death).
Atherosclerosis is considered a systemic disorder that uniformly affects all major blood vessels in the body. Hardening of the arteries can lead to softening of the penis because stiffened arteries can’t relax, open wide, and let the blood flow. Thus erectile dysfunction may just be the flaccid “tip of an iceberg” in terms of a systemic disorder. For two-thirds of men showing up to emergency rooms for the first time with crushing chest pain, their penis had been trying to warn them for years that something was wrong with their circulation.
Why does it hit the penis first? Because the penile arteries in the penis are half the size of the coronary artery in our heart. So the amount of plaque we wouldn’t even feel in the heart could clog half the penile artery, causing symptomatic restriction in blood flow. That’s why erectile dysfunction has been called “penile angina.” In fact, by measuring blood flow in a man’s penis we can predict the results of his cardiac stress test with an accuracy of 80%. Male sexual function is like a penile stress test, a “window into the hearts of men.”
Forty percent of men over age forty have erectile dysfunction. 40 over 40. Men with erection difficulties in their 40s have a 50-fold increased risk of having a cardiac event (like sudden death). I said before that various things increase heart disease risk by 20% or 30%. That’s nearly 5000%, leading the latest review to ask, “is there any risk greater?” That’s because it’s not so much a risk factor for atherosclerosis as atherosclerosis itself. A man “with erectile dysfunction (even if he doesn’t have cardiac symptoms) should be considered a cardiac patient until proven otherwise.”
Erectile dysfunction is considered to be a cardiac equivalent; it’s a marker of the coronary artery one likely already has. Thus, there’s more to treating ED than establishing an erect penis; it offers an opportunity for reducing cardiovascular risk. The reason even young men should care about their cholesterol is because itpredicts erectile dysfunction later in life, which in turn predicts heart attacks, strokes, and a shortened lifespan.
May 20, 2014 by Michael Greger M.D.
Anthony Atala’s state-of-the-art lab grows human organs — from muscles to blood vessels to bladders, and more. At TEDMED, he shows footage of his bio-engineers working with some of its sci-fi gizmos, including an oven-like bioreactor (preheat to 98.6 F) and a machine that “prints” human tissue.
Targeting pathway may lead to better hypertension treatments for at-risk patients
Obesity, heart disease, and high blood pressure (hypertension) are all related, but understanding the molecular pathways that underlie cause and effect is complicated.
A new University of Iowa study identifies a protein within certain brain cells as a communications hub for controlling blood pressure, and suggests that abnormal activation of this protein may be a mechanism that links cardiovascular disease and obesity to elevated blood pressure.
"Cardiovascular diseases are the leading cause of death worldwide, and hypertension is a major cardiovascular risk factor," says Kamal Rahmouni, UI associate professor of pharmacology and internal medicine, and senior study author. "Our study identifies the protein called mTORC1 in the hypothalamus as a key player in the control of blood pressure. Targeting mTORC1 pathways may, therefore, be a promising strategy for the management of cardiovascular risk factors."
The hypothalamus is a small region of the brain that is responsible for maintaining normal function for numerous bodily processes, including blood pressure, body temperature, and glucose levels. Signaling of mTORC1 protein in the hypothalamus has previously been shown to affect food intake and body weight.
The new study, which was published April 2 in the journal Cell Metabolism, shows that the mTORC1 protein is activated by small molecules and hormones that are associated with obesity and cardiovascular disease, and this activation leads to dramatic increases in blood pressure.
Leucine is an amino acid that we get from food, which is known to activate mTORC1. The UI researchers showed that activating mTORC1 in rat brains with leucine increased activity in the nerves that connect the brain to the kidney, an important organ in blood pressure control. The increased nerve activity was accompanied by a rise in blood pressure. Conversely, blocking this mTORC1 activation significantly blunted leucines blood pressure-raising effect.
This finding may have direct clinical relevance as elevated levels of leucine have been correlated with an increased risk of high blood pressure in patients with cardiovascular disease.
"Our new study suggests a mechanism by which leucine in the bloodstream might increase blood pressure, Rahmouni says.
Previous work has also suggested that mTORC1 is a signaling hub for leptin, a hormone produced by fat cells, which has been implicated in obesity-related hypertension.
Rahmouni and his colleagues showed that leptin activates mTORC1 in a specific part of the hypothalamus causing increased nerve activity and a rise in blood pressure. These effects are blocked by inhibiting activation of mTORC1.
Our study shows that when this protein is either activated or inhibited in a very specific manner, it can cause dramatic changes in blood pressure, Rahmouni says. "Given the importance of this protein for the control of blood pressure, any abnormality in its activity might explain the hypertension associated with certain conditions like obesity and cardiovascular disease."
Rahmouni and his team hope that uncovering the details of the pathways linking mTORC1 activation and high blood pressure might lead to better treatments for high blood pressure in patients with cardiovascular disease and obesity.
The research was funded by the National Institutes of Health (HL084207 and HL014388), the American Diabetes Association, and the Fraternal Order of Eagles Diabetes Research Center at the UI.
In addition to Rahmouni, the UI team included Shannon Harlan, Deng-Fu Guo, Donald Morgan, and Caroline Fernandes-Santos.
Kamal Rahmouni, Pharmacology, 319-353-5256
Jennifer Brown, UI Health Care Marketing and Communications, 319-356-7124
Jennifer Brown | Quelle: EurekAlert!
Weitere Informationen: www.uiowa.edu