Many men with low testosterone levels do not receive treatment

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The majority of men with androgen deficiency may not be receiving treatment despite having sufficient access to care, according to a report in the May 26 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.

Androgen deficiency in men means the body has lower than normal amounts of male hormones, including testosterone, according to background information in the article. Although prescriptions for testosterone therapy for aging men have increased in recent years, treatment patterns for androgen deficiency are not clearly understood in community-dwelling U.S. males.

Susan A. Hall, Ph.D., of New England Research Institutes, Watertown, Mass., and colleagues examined data collected from 1,486 Boston-area men (average age 46.4) from April 2002 to June 2005 to estimate the number of men receiving treatment for androgen deficiency, to explain how treated and untreated men varied in seeking care and to understand potential barriers to health care. Specific symptoms of androgen deficiency include low libido, erectile dysfunction and osteoporosis and less-specific symptoms include sleep disturbance, depressed mood and tiredness.

A total of 97 men met the criteria for having androgen deficiency. Eighty-six men were symptomatic and untreated, and 11 were prescribed testosterone treatment. “Men were using the following: testosterone gel (n=1), testosterone patch (n=3), testosterone cream (n=1), testosterone cypionate [an injectable form of testosterone] (n=1) or unspecified formulations of testosterone (n=5),” the authors write. “All of the unspecified forms of testosterone used were self-reported as administered in intervals defined in weeks, which suggests that these were injectable formulations.”

“Men with untreated androgen deficiency were the most likely of the three groups to have low socioeconomic status, to have no health insurance and to receive primary care in an emergency department or hospital outpatient clinic,” the authors write. However, all men with treated and untreated androgen deficiency were more likely to report receiving regular care than those without the condition and reported visiting their doctor more often throughout the year (with averages of 15.1 visits for those with untreated androgen deficiency, 6.7 visits for those without the condition and 12 visits for those with treated androgen deficiency).

“Under our assumptions, a large majority (87.8 percent) of 97 men in our groups with androgen deficiency were not receiving treatment despite adequate access to care,” the authors conclude. “The reasons for this are unknown but could be due to unrecognized androgen deficiency or unwillingness to prescribe testosterone therapy.”

Article Source: http://www.eurekalert.org/pub_releases/2008-05/jaaj-mmw052208.php

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Why the Kind of Body Fat You Carry Matters

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All fats are not created equal. We know this because we’re constantly correcting people who get it wrong. There are good fats and bad fats and really really bad fats and fats that are conditionally good or bad. Butter isn’t corn oil isn’t fish oil isn’t monounsaturated fat isn’t palmitoleic fat isn’t linoleic acid. Sometimes trans fat isn’t even trans fat. The same thing applies to the fat on your body. Depending on its location and composition, healthfulness isn’t distributed equally among adipose tissue. Some types of body fat are worse than others.

Fat is an endocrine organ. Like any other organ, it secretes hormones and other bioactive compounds that affect our physiology and determine our health.

Subcutaneous fat sits just below your skin. It’s the most conspicuous and least aesthetically-pleasing fat, comprising love handles and big droopy bellies, saggy arms and flabby necks, but it’s less actively harmful than many other types of body fat. Subcutaneous fat is the primary secretor of leptin, a strong regulator of appetite and metabolism, and of adiponectin, a marker for metabolic health with potentially anti-atherosclerotic effects.

Gluteofemoral fat is lower body fat, specifically the stuff that sits on your butt, hips, and thighs. In women, its presence indicates (and may even determine) good metabolic health. And it may not just be a signal for health, but an actor. Fat depots on the butt and hips actively secrete greater amounts of palmitoleic acid (PDF), a fatty acid with insulin-sensitizing effects. Gluteofemoral fat contains a greater proportion of omega-3 fatty acids, which are used to construct baby brains.

Visceral fat lies inside the abdominal cavity. It surrounds and envelops the organs. Contrasted with subcutaneous fat, visceral fat releases far less leptin and adiponectin. Instead, it secretes large amounts of IL-6, an inflammatory cytokine strongly correlated with systemic inflammation.

Intrahepatic fat is fat inside the liver. More than any other type of fat, intrahepatic fat is strongly associated with the metabolic complications of obesity.

Epicardial fat is visceral fat that surrounds the heart. If you’ve ever gotten a cow heart wrapped in hard yellowish fat, that’s epicardial fat. Large amounts of epicardial fat are associated with obesity, diabetes, and hypertension. And while epicardial fat appears to be primarily a signal of metabolic disturbances, it also exerts direct effects on heart function and releases inflammatory molecules that affect surrounding tissues.

Intermuscular fat lies between muscles. The less you use a muscle, the more it atrophies and the more fat will replace it. You may have seen the MRI of two thigh cross sections—one from a lifelong athlete and one from an age-matched couch potato. The athlete’s leg is a dense circle of bone surrounded by several inches of lean muscle in each direction followed by a small layer of fat. The sedentary leg is smaller circle of bone surrounded by a mishmash of marbled meat with several inches of thick white fat. Delicious and tender when seared, I’d imagine, but terrible for the person’s health and ability to function.

Intramuscular fat lies inside the muscles. Kobe beef steaks have lots of intramuscular fat. It’s the marbling, the presence of fat between muscle fibers. If you actually utilize it, intramuscular fat provides a nice source of energy for the muscles. Then again, if you were using your muscles in the first place it’d be tough to accumulate much intramuscular fat. The quickest way to get rid of intramuscular fat is with low-level aerobic activity. Staying under 75% of max heart rate will keep you burning predominately fat, and exercising while on a ketogenic diet is an even better way to do it; nutritional ketosis increases exercise-induced intramuscular fat oxidation 20-fold.

Brown fat isn’t really fat. It is, but it isn’t. Like muscle, it’s highly metabolically active. We use it to generate heat (thus burning energy) in response to cold exposure. Babies have a ton of brown fat, since they can’t shiver to stay warm, and until recently researchers assumed adults didn’t have much at all. Now we know that’s wrong. Cold plunges, swimming in cool water, and even going outside in short sleeves and shorts in cold weather can all stimulate the formation of brown fat in adults (I wouldn’t advise dunking your newborn in an ice bath for the health benefits). Those jerk babies aren’t the only ones enjoying that sweet, sweet brown fat after all.

Best of all, “training” for brown fat—in one study, exposing yourself to cool weather (60°F) for just 2 hours a day for six weeks while wearing light clothing—can increase energy expenditure and reduce overall body fatness. That’s not even a big dose of cold. Forgetting your jacket at home is probably enough.

Different populations have different body fat distribution patterns. Let’s look at a few:

South Asians (Indians, Pakistanis, Bangladeshis) have smaller subcutaneous “reservoirs” than whites, so a larger proportion of weight gain in this population diverts to visceral—and more dangerous—fat stores. Dr. Ron Sinha wrote about this (and still does on his blog) in the fantastic South Asian Health Solution.

Compared to Australian whites, Japanese men have more body fat for a given BMI.

Black Americans have less visceral fat and more subcutaneous fat for a given BMI than white Americans (PDF). Oddly, this doesn’t translate to a lower risk of diabetes.

Australian Aborigines have more trunk fat and less limb fat for a given BMI than Australians of European descent. Aborigine women have higher waist circumferences and waist:hip ratios than Aussie European women for a given BMI.

Men and women carry fat differently. I mentioned that briefly above in the section on gluteofemoral fat, and I covered the differences extensively in a previous post. Go read that now. In short, men are more likely to store fat on the trunk and around the waist, leading to the fat-guy-with-stick-legs syndrome. Women tend to store fat in the butt, thighs, and hips. Upon reaching menopause, women stop producing as much estrogen and begin storing more fat in the waist and abdomen.

The eternal question persists: is it cause or signal? Risk factor or actor? For most of these types of fat, the answer is probably “both.” Fatty liver indicates metabolic dysfunction, but it can also impair the liver’s functions and lead to insulin resistance and eventually diabetes. People with lots of brown fat may be lean and healthy because they spend a lot of time being active in cold weather, but the brown fat also increases caloric expenditure. Large amounts of intramuscular and epicardial fat indicate a sedentary lifestyle, which is damaging in its own right, but the fat secretes inflammatory compounds with real biological effects.

Teasing apart which link along the chain of causality is to blame is probably impossible. That doesn’t mean we can’t make a few safe recommendations.

Women shouldn’t stress out about a little butt, hip, and thigh fat. It’s likely a good sign.

Belly fat is bad. Fat around your heart is bad. Fat in your liver is bad. Subcutaneous fat looks bad and is hardest to burn but might not be too unhealthy. Losing weight will reduce all of it.

To target belly fat, intense training works best. The resultant spike in catecholamines will preferentially target visceral fat. Just be sure to get enough sleep, rest, and recovery, as chronic stress and under-recovery tends to chronically elevate the catecholamines and make belly fat more stubborn.

To target liver fat, limit sugar, eat lots of choline (from yolks and liver), and practice high intensity interval training. When you drink alcohol, make sure you protect your liver with saturated fat (beef, cocoa, coconut fat all protect against alcohol-induced fatty liver).

To target intramuscular fat, exercise in a low-carb or ketogenic state. Nothing too intense is required. A long, reasonably intense hike (lots of hills) on an empty stomach twice a week might do the trick.

To target epicardial fat, exercise. Both intense and moderate-intensity training seem to work.

To get more brown fat, forget your jacket. Heck, burn it. Just don’t stand too close to the fire.

If it sounds confusing, it shouldn’t. The basics apply. Recommendations haven’t changed. I just find all the different types of fat incredibly interesting. Don’t you?

Written By: Mark Sisson
Read more: http://www.marksdailyapple.com/why-the-kind-of-body-fat-you-carry-matters/#ixzz4CySo9miq

 

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How Your Gut Controls Your Brain

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Whether you’re suffering from anxiety or are just in a crabby mood, before you start poking around your head as if looking for answers, you might do well to aim a little lower: your gut.

“Do you have gut instincts? Do you get butterflies in your stomach when you’re nervous? Can a job interview cause you to have stomach cramps?” asks Elizabeth Lipski, PhD, CCN, CHN, author of Digestion Connection. “These things happen because your nervous system and digestive system are intertwined.”

The connection between the brain and the gut is called the gut-brain axis, and it’s a two-way street. “The gut and the brain and the brain and the gut are intimately connected in a bi-directional way,” says David Perlmutter, MD, author of Brain Maker. “We’re just beginning to understand that this incredible relationship exists between our digestive system and the brain.”

While science is just catching up to the idea that the brain and the gut are more intertwined than we ever imagined, this idea has been appreciated by natural practitioners for a long time.

“Many years ago, naturopaths and holistically oriented doctors understood that bacterial imbalances were problematic,” says Gerard Mullin, MD, author of The Gut Balance Revolution. “They knew that to get healthy you had to rebalance the gut bacteria. But modern science, which is very pill oriented, has been proactively dismissive of these things and felt it was predicated on quackery. Now the evidence is so overwhelming, and more and more people appreciate it.”

Here’s some of the evidence that experts are pointing to when it comes to the complicated relationship between your brain and belly.

Mood
“It’s a bit humbling, this information, but the fact is, more than 90 percent of the neurotransmitters—chemicals like dopamine and serotonin, that actually serve to regulate our mood—are made in the gut,” says Dr. Perlmutter.

He explains that it’s the bacteria themselves that play an important role in the very manufacture of these neurotransmitters. If your gut is populated with the wrong bugs, they won’t be able to make the same feel-good chemicals, which can have a major impact on your mood.

Depression
In fact, these gut bacteria play such an important role in creating these neurotransmitters that an imbalanced gut is even linked to depression. “The reason people take antidepressants is to elevate levels of serotonin in the brain; and yet, the target here is the gut, not the brain, because the gut is where these chemicals come from in the first place,” says Dr. Perlmutter

Depression is also an inflammatory condition. And the first place to start looking for inflammation is in the gut.

“When there’s an imbalance in your gut bacteria, that is going to create shifts in your expression of gut hormones,” says Dr. Mullin. “It’ll cause the gut lining to become more permeable. That will allow the bacterial toxins to disseminate and cause an inflammatory reaction, which can affect brain function adversely.”

Anxiety
Similarly to depression, an imbalanced gut may also be at the root of anxiety. Research published in Psychiatry Research found that those who ate more probiotic-rich fermented foods were less likely to experience social anxiety.

Cognitive Function
That foggy feeling you get after eating too much junk food isn’t in your head—it’s in your gut. “If I had to choose one word that I hear from my patients, it’s ‘clarity,'” says Dr. Perlmutter, describing what happens when people rebalance their gut. “A lot of what we hear from patients is, ‘The fog was lifted.’ People didn’t realize there was fog until it has lifted and they become clear.”

Research from Oregon State University supports this anecdotal reaction. They found that mice fed a high-fat, high-sugar diet saw a shift in gut bacteria that was linked to a loss of cognitive flexibility (the ability to adapt to changing situations) and short- and long-term memory.

Dr. Perlmutter explains that the wrong gut bacteria can lead to “static on the line,” as he puts it. “The brain has got to receive plenty of energy to function. In the presence of inflammatory chemicals, the brain is less efficient at creating energy and it doesn’t work as well,” he says. “What happens in that situation is you develop static on the line. Your bandwidth goes down. It’s taking longer and longer to load those mental websites, if you will. And understand that gut bacteria are the mediators of inflammation throughout the body, including in the brain.”

Cravings and Recognizing Fullness
There’s a small part of your head that says, “I don’t need that french fry,” but the much louder message is, “More!” Turns out that the foods you put into your stomach affect how your brain looks at the rest of your meal.

Research from the Society for the Study of Ingestive Behavior found that feeding rats a high-fat diet led to gut bacteria shifts and caused the brain to fail to receive the “I’m full” message from the belly.

“The brain is changed by eating unbalanced foods,” explains Krzysztof Czaja, DVM, PhD, a principal investigator on the study and associate professor of neuroanatomy at the University of Georgia College of Veterinary Medicine. “It induces inflammation in the brain regions responsible for feeding behavior. Those reorganized circuits and inflammation may alter satiety signaling.”

Plus, bacteria may also be at the helm when it comes to steering you toward healthy—or unhealthy—choices. Research published in BioEssaysfound that microbes are able to manipulate us into eating things that they want to eat—and bad bacteria crave junk food. These germs are able to manipulate taste receptors, make us feel bad, or send out rewards to control the foods we send into our stomachs.

Skeptical that a tiny little germ could control your behavior? Dr. Perlmutter explains that gut microbes are so powerful that they can make a rat fall in love with a cat (and then promptly get eaten). The toxoplasmosis organism lives inside the digestive tract of a cat, and it would like to stay there. However, the cat will ultimately excrete the germ in its feces. To get back into the cat, the microbe manipulates whatever host picks it up—in this instance, a rat.

“When a rodent is infected with toxoplasmosis organism, the bacteria changes the brain of the rodent so that it begins to see the cat as a sexual partner,” says Dr. Perlmutter. Presenting itself as a mate to a cat is a surefire way to get that rodent eaten. “The cat then gobbles it up,” he says.

“How powerful an example is that that the germ is manipulating its host (the rodent) in order to continue its life cycle?!”

Written by: JULIA WESTBROOK

Article Source: http://www.rodalewellness.com/health/how-your-gut-controls-your-brain

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Dose of nature is just what the doctor ordered

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People who visit parks for 30 minutes or more each week are much less likely to have high blood pressure or poor mental health than those who don’t, according to new research by Australian and UK environmental scientists.

A study led by The University of Queensland (UQ) and the ARC Centre of Excellence for Environmental Decisions (CEED) suggests people might need a minimum “dose of nature”.

UQ CEED researcher Dr Danielle Shanahan said parks offered health benefits including reduced risks of developing heart disease, stress, anxiety and depression.

“If everyone visited their local parks for half an hour each week there would be seven per cent fewer cases of depression and nine percent fewer cases of high blood pressure,” she said.

“Given that the societal costs of depression alone in Australia are estimated at $A12.6 billion a year, savings to public health budgets across all health outcomes could be immense,” she said.

UQ CEED researcher Associate Professor Richard Fuller said the research could transform the way people viewed urban parks.

“We’ve known for a long time that visiting parks is good for our health, but we are now beginning to establish exactly how much time we need to spend in parks to gain these benefits,” he said.

“We have specific evidence that we need regular visits of at least half an hour to ensure we get these benefits.”

Dr Shanahan said 40 per cent of Brisbane residents did not visit an urban park in a typical week.

“So how can we encourage people to spend more time in green space?” she said.

“We need more support and encouragement of community activities in natural spaces.

“For example, the Nature Play programs in Queensland, Western Australia and South Australia provide heaps of ideas for helping kids enjoy the great outdoors.

“Our children especially benefit from spending more time outdoors. Kids who grow up experiencing natural environments may benefit developmentally and have a heightened environmental awareness as adults than those who don’t.”

The research is published in Nature Scientific Reports. The research team included scientists from UQ’s School of Public Health, the University of Exeter, and CSIRO Land and Water.

Article Source: http://www.eurekalert.org/pub_releases/2016-06/uoq-don062316.php

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Middle-aged men: Could dwindling testosterone levels decrease sleep?

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At 30 years old, male testosterone levels drop by one to two percent annually. By age 40, men’s quality of sleep begins to diminish. Could there be a link between decreased testosterone and reduced sleep? Absolutely according to Zoran Sekerovic, a graduate student from the University of Montreal Department of Psychology, who presented his findings at the annual conference of the Association francophone pour le savoir (ACFAS).

Sekerovic discovered a link between testosterone levels in men over 50 and their quality of sleep – specifically less deep sleep i.e. Phases III and IV of the slumber cycle. “Deep sleep is when the recuperation of body and mind is optimal,” says Sekerovic, adding his is the first study to find this correlation.

In young men, deep sleep represents 10 to 20 percent of total sleep. By age 50, it decreases to five to seven percent. For men over 60, it can disappear altogether. The study didn’t find any correlation with other parts of the sleep cycle: falling asleep, Phases I and II, or paradoxical sleep, when most of dreaming occurs.

The University of Montreal researcher explains that men in their 20s don’t have such a correlation because their neuronal circuits are intact. “With age, there is neuronal loss and the synchronization of cerebral activity isn’t as good, which is why there is a loss of deep sleep. Because deep sleep requires great synchronization,” says Sekerovic. “Low levels of testosterone intensify the lack of synchronization and can explain 20 percent of men’s inability to experience deep sleep.”

Sekerovic suggests dwindling testosterone levels are what impact sleep, not vice-versa, as other studies have suggested. He adds previous investigations measured daily fluctuations in testosterone levels, which are higher in the morning.

If Sekerovic is right, his findings could re-ignite the hormone therapy debate. “The loss of deep sleep is a serious problem that could be treated with testosterone. That would be tremendous progress,” says Sekerovic. “But hormone therapy can have secondary effects. Therefore, it will be essential to better understand the mechanisms leading to the loss of deep sleep.”

This study was conducted under the supervision of Julie Carrier, a professor of psychology at the University of Montreal and director of the Chronobiology Laboratory at the Hôpital du Sacré-Coeur de Montréal.

Article Source: http://www.eurekalert.org/pub_releases/2010-05/uom-mmc051410.php

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FACTS ABOUT DIM AND MEN’S HEALTH

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Several classes of chemical compounds which naturally occur in fruits and vegetables possess anticarcenogenic properties. The cruciferous vegetables, such as cabbage and broccoli are particularly rich sources of such compounds, including Indole derivatives [indole-3-carbinol (I3C) and indole-3-acetonitrile], dithilthiones and isothiocyanates. Increased consumption of cruciferous vegetables is associated with reduced tumor incidents in humans and experimental animals.

Diindolylmethane (DIM, in short) is the principal breakdown product of indole 3-carbinol (I3C), the phytochemical found in cruciferous vegetables like cabbage, cauliflower, broccoli, brussel sprouts, kale, collards, mustard greens, radishes, watercress, and turnips. DIM, has been shown in scientifi­c studies to reduce the risk of prostate and other hormone-driven cancers by helping the body to make a better balance of the hormones.*

Can taking 250 – 300 mg. of DIM (or its equivalent in raw cruciferous vegetables) reduce your risk for prostate cancer?
Yes, according to Dr. Michael Zeligs, M.D. author of All About DIM. “A recent study of Seattle men showed that three or more servings of cruciferous vegetables a week can reduce prostate cancer risk almost by half.” His statement is based on an article by J. H. Cohen, et. al. Fruit and vegetable intakes and prostate cancer risk. Natl. Cancer Inst. Jan 2000; 5;92 (1): 61-8.

The following quotations are taken from All about DIM by Michael A. Zeligs, M.D. and A. Scott Connelly, M.D., based on research related to men’s use of diindolylmethane (DIM) and the phytochemical compounds (indole-3-carbinol) found in cruciferous vegetables from which DIM is derived.  Following the quotations is a partial bibliography substantiating the claims made in the article.

DIM & Testosterone

What is Testosterone?

Testosterone is an important contributor to healthy hormonal balance in both men and women. Testosterone is known as an androgen because when its effect dominate male characteristics are seen. These include male distribution of body hair, a deeper voice, and male genital development. Testosterone is also identified as anabolic hormone due to its ability to promote protein synthesis. Active protein synthesis produce bigger muscles and stronger bones, especially in response to exercise. This process also increase metabolic rate and consumes fat, resulting in a leaner physique. The more subtle effects of testosterone have to do with its action as a support for mood and libido. Testosterone has a clear anti-depressant action and promotes interest in sex and men and women.

How does DIM benefit testosterone activity?

Testosterone acts differently depending on whether it is free or bound to carrier proteins in the blood. DIM, through its effects on estrogen metabolism supports testosterone by helping to maintain the level of free or active testosterone. Free testosterone refers to defraction of testosterone that circulates in the blood and is not associated with or bound by SHBG (Sex Hormone Binding Globulin), its carrier protein. Since only free testosterone easily crosses into the brain, muscles, and fat cells much of the desirable action of testosterone has to do with the free portion. However, this represents only a tiny amount of the total testosterone equal to only to 2% of the total in men and even less in women.

High levels of SHBG lock up free testosterone making it unavailable to support mood or metabolism. Interestingly, unmetabolized estrogen is the body’s primary signal to increase the production and levels of the testosterone-binding protein. Low levels of free testosterone have been identified during perimenopause and are most dramatic in women with severe premenstrual syndrome (PMS) symptoms. (24)

How can DIM help with age-related reduced levels of free testosterone?

Since DIM promotes a more active metabolism of estrogen, unmetabolized estrogen levels fall and the 2-hydroxy-estrogens increase. The 2-hydroxy-estrogens possess the unique ability to displace testosterone from SHGB and set it free. Therefore, the combined effect of DIM to reduce unmetabolized estrogen and increase 2-hydroxy-estrogens can reduce elevations in SHGB and allow for more free testosterone. Both of these changes help maintain and restore a youthful balance between estrogen and free testosterone. This balance is a key to a healthy and active metabolism. (25)

Does DIM help maintain a healthy testosterone level in older men?

Zelligs: “The same dynamics for maintaining higher total and free testosterone levels apply to healthy aging in men.  Estrogen metabolism is slowed during aging in men, especially in association with obesity and regular alcohol use.” [translation: As we age, our bodies take longer to “clear” the estrogen in our cells and higher than healthy levels of estrogen are common, especially in men who are obese or who are regular social drinkers.]

“Avoiding overactive testosterone metabolism, [clearing the testosterone too quickly] and reducing the conversion of testosterone into estrogen are goals of nutritional support in middle aged and older men.”

“It is well documented that estrogen accumulates in the prostate gland starting at age 50 (42) and that estrogen is associated with the degree of prostate enlargement. (43)

“Based on animal and human testing, DIM is again preferable to I3C in the area of men’s health.  Using DIM in men avoids accelerating testosterone metabolism, especially regarding unwanted conversion of testosterone into estrogen.”

Does DIM help improve prostate health and reduce night time urination in older men?

“Regarding men’s health, supplementation with absorbable DIM has resulted in reports of improved prostate function based on reduced nighttime urination in symptomatic older men.”

“Once absorbed, DIM is uniquely active in promoting healthy estrogen metabolism and improving symptoms of estrogen-related imbalance in both men and women.”

“Apart from therapeutic potential, dietary supplement use of DIM and I3C relates to hormonal balance and symptoms of “estrogen dominance.”

Even more impressive is research showing that unmetabolized estrogen accumulates in prostate tissue in men as they age. Exposure of human prostate tissue to unmetabolized estrogen in the laboratory did indeed result in activation and increased production of prostate specific antigen protein (PSA). The PSA protein level in men’s blood is now used as a screening test to determine the severity of prostate enlargement or to determine the chance of prostate cancer. Recent studies also have shown that estradiol, the active form of estrogen, causes the prostate gland to increase its production of prostate specific antigen (PSA). Increased PSA production, however, can be inhibited by the “good” estrogen metabolites promoted by DIM. This indicates that “good” estrogen metabolites are more beneficial for prostate health than unmetabolized estrogen-like estradiol. (53)

Various supplements, including DIM, can now be used to reduce the risk of prostate enlargement and promote a healthy prostate. Optimum testosterone-2-estrogen hormonal balance achieved with the use of DIM can help to preserve a youthful urinary tract, prevent age-related prostate growth, and perhaps reduce the risk of prostate cancer.

Long term safety has been demonstrated in DIM.

Article source: https://wholeworldbotanicals.com/facts-about-dim-and-mens-health/

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Fish and Prostate Cancer Risk: Fact or Fiction

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Several scientific studies have found a reduction in prostate cancer associated with increased omega-3 intake.1-11 A recent report purportedly showed the opposite.12

This report was based on a single blood test of plasma fatty acids in a group of 834 men who were followed up to six years to assess prostate cancer risk (low- and high-grade disease). A smaller group of 75 men was followed up to nine years to assess only high-grade prostate cancer risk.

The results showed that slightly higher omega-3 plasma percentages from this single blood test were associated with a greater risk of low-grade (44%) and high-grade (71%) prostate cancers over the multi-year follow-up.

This report was turned into news stories with headlines blaring “Omega-3 fatty acids may raise prostate cancer risk.

Omitted from the media frenzy was the fact that this study was not about fish oil supplementusers. The authors admitted they did not know how the study participants achieved what turned out to be very low omega-3 plasma percentages in all groups.

In fact, omega-3 plasma levels were only about 40% of what would be expected in health conscious people taking the proper dose of fish oil.12 ,13 The insufficient levels of plasmaomega-3s in all the study subjects were overlooked by the media. Had these very low plasma levels of omega-3s been recognized, it would have been apparent that this report had no meaning for those who boost their omega-3 consumption through diet and supplements.

Also absent from the reporting was that more men with slightly higher omega-3 plasma levels had confounding risk factors for greater risk of contracting prostate cancer at baseline, such as having higher PSA scores and a positive family history. Although the authors attempted to statistically control (through a statistical model called multivariate analysis) for some of these risk factors in their analysis, the concern remains that the baseline data was confounded and therefore the statistical analysis invalid, and that the reported results are compromised by higher rates of preexisting disease along with a genetic predisposition, not because of the minuscule variance in the amount of their plasma omega-3.

Prostate cancer sharply increases by 120% to 180% in men who have a first-degree relative who had contracted prostate cancer. Nearly double the men who contracted prostate cancer in this study had a positive family history, and although the researchers attempted to statistically control for this confounding factor, this fact was conveniently overlooked by the mainstream media asomega-3s were instead labeled the culprit.

Associating a one-time plasma omega-3 reading with long term prostate cancer risk is ludicrous. That’s because plasma omega-3 changes rapidly with short-term dietary changes. It does not reflect long-term incorporation of omega-3 into cells and tissues. In this report, differences in baseline omega-3 blood measures were so trivial that if a man had just one salmon meal the night before, he could have wound up in the “higher” omega-3 group even if he never ingested another omega-3 again.14

Numerous flaws in this report render its findings useless for those who supplement with purifiedfish oils and follow healthy dietary patterns. This article represents Life Extension®’s initial rebuttal to this spurious attack on omega-3s that was blown out of proportion by the media.

Prostate cancer is a slow developing malignancy that can take decades to manifest as clinically-relevant disease. Commonly recognized risk factors for contracting prostate cancer are diet, body mass, race, family history, hormone status, and age.15,16

An under-recognized risk factor associated with developing prostate cancer is coronary artery disease.17We at Life Extension long ago observed that men with clogged coronary arteries often developed prostate cancer (and vice versa). A renowned prostate oncologist named Stephen Strum, M.D., made a similar observation and established a common factor behind coronary heart disease and prostate cancer, i.e., bone loss.

Coronary artery disease is clearly linked with osteoporosis,18 as lack of vitamin K prevents calcium from binding to bone and instead allows it to infiltrate and harden the arteries. The ensuing bone loss results in the excessive release of bone-derived growth factors that fuel prostate cancer propagation and metastasis.

Long after Dr. Strum published his elaborate correlation, a 2012 study of 6,729 men showed coronary artery disease to be associated with a 35% increased risk of prostate cancer.17

The reason we bring up the connection of heart disease and prostate cancer is that the authors of the controversial study apparently failed to assess overall baseline health status of the study subjects. We initially suspected that men in the higher group of plasma omega-3 (which turned out to be low by our standards) were more likely to have coronary heart disease. That’s because men with heart disease are told by their cardiologists to eat less red meat and more cold-water fish. So it would not be surprising if the plasma percentage of omega-3 was higher in men with prostate cancer as they may have been trying to eat healthier to avoid bypass surgery or a sudden heart attack.

When we asked the authors of the report if they assessed the baseline cardiovascular status of the subjects, their reply was, No, I don’t believe this to be the case.

Family History Predisposition

If your father or brother develops prostate cancer, your odds of getting it are about 120% to 180% greater than if you don’t have this family history.19

In the report attacking omega-3s, men who contracted prostate cancer had almost double the proportion of first-degree relatives with a history of prostate cancer compared with controls. Although the study authors apparently attempted to control for this baseline risk factor through the use of statistical modeling of selected variables (multivariate analysis), this confounding factor calls into question much of this report’s negative findings, but was not even mentioned in the media’s rush to create headline grabbers.

Men with a family history of prostate cancer often have witnessed the long term death spiral that prostate cancer patients suffer through. As a result, they attempt to adapt healthier lifestyles to avoid becoming a victim of their hereditary genes.

Since eating well-done red meat has long been associated with increased prostate cancer risk, men with unfavorable family histories are more likely to include at least some cold-water fish in their diets, and therefore have higher omega-3 percentage plasma levels. This does not mean the marginally higher omega-3 caused their prostate cancer.

This is partially corroborated with the data from the study participants who did not develop prostate cancer, but had higher plasma percentage levels of pro-inflammatory omega-6 fats. This indicated these individuals had little concern about what they ate since they had about half the family history rate of prostate cancer.

Fortunately there may be ways to alter family history genetic predispositions for prostate cancer by eating lots of cruciferous vegetables, maintaining youthful hormone balance, ensuring optimal vitamin D status, and taking compounds that favorably alter gene expression like metformin and curcumin.20-28

Baseline PSA Higher in Those Who Contracted Prostate Cancer

Prostate specific antigen (PSA) is a blood marker of prostate disease.

Standard laboratory reference ranges often allow PSA to reach 4.0 ng/mL before flagging a potential problem. A more progressive view of the PSA is that any number over 2.4 ng/mL should be viewed with suspicion, with a digital rectal exam performed and a follow-up PSA blood test done in three months.

Life Extension has published comprehensive articles about how to properly interpret PSA results, but to state it succinctly: Aging men with PSA readings greater than 2.4 ng/mL are at higher risk for developing clinically relevant prostate cancer and should initiate aggressive steps to reverse the underlying process.

In the report that associated higher omega-3 blood levels with increased prostate cancer incidence, 41.1% of the men who went on to develop prostate cancer had baseline PSA readings greater than 3.0 ng/mL. In the group that did not develop prostate cancer, only 7.3% has a PSA baseline reading greater than 3.0 ng/mL.

Although the study researchers attempted to statistically control for other confounding factors in their analysis like family history, age, and education level, this PSA finding implies that many of the men who developed prostate cancer already had it (pre-existing disease) when the baseline plasma omega-3 level was measured. This finding of 5.6 times more men who developed prostate cancer with a baseline PSA level greater than 3.0 ng/mL compared to the “no cancer” group is impossible to rationally discount. To reiterate, below is the data on the baseline PSA readings from the report the media used to discredit omega-3s:

  • 7.3% of the “No Cancer” group had PSA of ≥3.0
  • 41.1% of the “Total Cancer” group had PSA of ≥3.0

This critical piece of data was ignored in the tabloid-like media articles that erroneously blamed the increase in prostate cancer on omega-3s.

Study Subjects do not Appear to Have Taken Fish Oil Supplements

Life Extension scientists repeatedly reached out to the authors of the negative report, but did not receive a response as to whether any attempt was made to ascertain the source of the omega-3 in the study subjects’ blood. We wanted to know if these men regularly ate cold-water fish or took at least some fish oil supplements.

Despite our requests, no clarification was made available by study authors as to the level of dietary supplementation with fish oil, and if so, the source of fish oil used in the study.

Based upon the very low plasma percentage levels of omega-3 fatty acids detected in the study, the implication is that dietary supplementation with fish oil likely did not occur. Instead, based upon the low levels of omega-3 plasma phospholipids detected, the source appears to have been primarily (potentially exclusively) diet only. As we will show soon, it appears that none of the men in this study consumed much in the way ofcold-water fish either.

Omega-3 Levels Were Low in All Study Subjects

You will be shocked to learn how low the average plasma percentages of omega-3 were in all these study subjects, whether they were in the high or low rate of prostate cancer group.

Plasma phospholipid testing for fatty acids was used in this study. However, this type of fatty acid testing can vary widely depending upon short-term dietary intake. In contrast, long-term uptake by cells and tissues of the body is far less dependent upon short-term changes in diet. For this reason, erythrocyte (red blood cell) fatty acid indices are far better at evaluating cellular uptake over time as a result of fish ingestion and fish oil supplementation.

For example, data indicates that supplementing with about 2 grams of omega-3 fatty acids from fish oil leads to an increase in erythrocyte (red blood cell) omega-3 fatty acid percentage from about 4% at baseline to about 8% at eight weeks.13

In a case analysis conducted by Life Extension staff, a healthy diet that included fish but not fish oil supplementation resulted in an omega-3 red blood cell (RBC) equivalence level of 6.06%.

However, a standard diet supplemented with 3.6 grams of EPA/DHA from purified fish oil resulted in an omega-3 RBC equivalence level of 10.59%. Thus, compared to what can be achieved with a healthy diet alone, adding a high quality fish oil supplement can nearly double a person’s omega-3 RBC equivalence score, which is consistent with the published literature.

Therefore, if participants in the report alleging an association with fish and prostate cancer had been taking meaningful doses of fish oil supplements, their levels should have been substantially higher than what the study authors reported. Instead, for men in the prostate cancer group of this study, the percentage of plasma long-chain omega-3 fatty acids was only 4.66% … a lower level than historic baselines taking no supplemental omega-3s.13

The numbers below should clarify this glaring flaw that renders conclusions from this report claiming fish or fish oil increases prostate cancer utterly meaningless:

  • Omega-3 RBC equivalence percentage of a moderate fish eater: 6.06%
  • Omega-3 RBC equivalence percentage when taking 3.6 grams/day EPA/DHA: 10.59%
  • Average long-chain omega-3 plasma percentage in study group with higher prostate cancer rates:4.66%
  • Average long-chain omega-3 plasma percentage in study control group (no prostate cancer): 4.48%
Comparison of Omega-3 Values

Figure 1: If you can’t see a difference in the two bars showing plasma percentage of omega-3s between men who contracted prostate cancer and those who did not, that’s because there is virtually no difference. The 0.18% variation could have resulted from men eating just a few ounces of fish the night before their one-time baseline blood draw. These low percentages of plasma omega-3s indicate these men were not taking fish oil supplements, nor were they eating much in the way of omega-3-rich foods in their diet.

There may be no need to provide any more rebuttal than the numbers posted above. They make it clear that the average subject in their groups were consuming very little cold-water fish and certainly no meaningful fish oil supplement. Their entire study population was so negligible in omega-3 that no relevant correlation can be drawn for health conscious people today choosing omega-3-rich foods (like cold-water fish) and high-potency fish oil supplements.

Yet based on this study of men who consumed relatively no omega-3s, frenzied news reporters were advising the public to stop eating cold-water fish and avoid omega-3 supplements.

Virtually No Difference in Omega-3 in Men Who Developed Prostate Cancer

When reading the frantic news reports, you would have thought the omega-3 difference in men with up to 71%increased risk of prostate cancer must have been huge.

At Life Extension, our very first reaction was that the researchers were comparing cardiac patients who gobbled down huge amounts of fish oil supplements to normal individuals who consume relatively little omega-3s. Our initial assumption was that since heart disease patients have higher prostate cancer rates, then that would explain why higher omega-3 could be mistakenly associated with increased prostate cancer risk, since heart disease patients are known to consistently take high-potencies of omega-3s through diet and supplements. How wrong our early conjecture was!

It turns out that the differences in omega-3 plasma phospholipid levels between groups were slight. In fact they were so close that we at Life Extension would classify them all as being too narrow to extrapolate meaningful data.

Our goal is to get the red blood cell (RBC) omega-3 index values in Life Extension members to 8%-11% as this level was shown to offer the greatest protection against sudden myocardial infarction, yet the average quartile for plasma long-chain omega-3 fatty acids in the prostate cancer cases in the report associating fish oil with prostate cancer was only 4.66%.

Now look how narrow the difference is between men with higher prostate cancer rates. In the group whose average baseline blood draw showed 4.48% plasma long-chain omega-3 fatty acids, there was no increased prostate cancer risk. But if the omega-3 percentage average went up to 4.66% (about 1/5 of one percent), prostate cancer rates skyrocketed, according to the report’s authors.

We’re talking here of a difference of 0.18% in the percentage of plasma omega-3 fatty acids that supposedly caused a 43% to 71% increase in prostate cancer incidence. Dedicated fish oil supplement users, on the other hand have over 100% higher omega-3 levels than seen in this study of men who apparently consumed little cold-water fish and no omega-3 supplements.

To put this into real-world perspective, the trivial difference (0.18%) in plasma omega-3 between men with no prostate cancer and those with prostate cancer could occur if a man ate just a few ounces of a cold-water fish like salmon the night before.

Remember, plasma phospholipid testing for fatty acids was used in this study. However, this type of fatty acid testing can vary widely depending upon short-term dietary intake. In contrast, long-term uptake by cells and tissues of the body is far less dependent upon short-term changes in diet. For this reason, the omega-3 RBC equivalence score is far better at evaluating cellular uptake over time as a result of fish ingestion and fish oil supplementation.

There was only one baseline blood draw. The men were followed up to six years (low-grade and high-grade cancer), with a smaller group followed up to nine years to see who would get high-grade prostate cancer. Those who developed prostate cancer were then compared against their baseline blood draw done years earlier.

This kind of methodology is open to misinterpretation and errors even if there were large variances in omega-3 fatty acid percentages, but the 0.18% difference is so tiny that it has no relevance to aging humans who choose to include omega-3-rich foods in their diet and supplement with fish oil.

This may be the first study that seeks to discredit a food/supplement (i.e., omega-3s), where the human subjects were not even taking a fish oil supplement nor ingesting significant amounts of an omega-3 food.

A 0.18% difference in plasma omega-3 fatty acids between men who contracted prostate cancer and those who did not is infinitesimally small. To extrapolate a conclusion from this very small difference that eating fish or taking fish oil supplements is risky, false, misleading, and meaningless … but it did generate a lot of news headlines.

Life Extension is concerned that some men will decrease consumption of omega-3s resulting in a devastating increase of their triglycerides, thrombotic, inflammatory and atherogenic risks. An epidemic of coronary artery blockage and ischemic stroke will soon follow.

Results Are Completely Inconsistent With the Known Biology, Pathophysiology, and Biochemistry of Prostate Cancer

A fundamental aspect of quality research is consistency, and repeatability.

Stated another way, for a medical finding to be considered valid, the results should not contradict well-established facts involving known biology, physiology, biochemistry, etc. Furthermore, the finding should be repeatable by other scientists.

The report attacking omega-3s is inconsistent with a variety of aspects of the well-established scientific and medical literature.

For example, upon close inspection of the data (and not simply a top-line, parroted response by the mainstream media eager to generate headlines), non-smokers had more aggressive prostate cancer, and non-drinkers (alcohol) had higher risk of prostate cancer, and prostate cancer case subjects were less likely to report a history of diabetes than controls.

Based upon these results, the implication is that men who wish to avoid prostate cancer should consume excess calories and develop diabetes, drink alcohol heavily, and abuse tobacco.

This is completely inconsistent with well-established science, and utter nonsense.

In fact, numerous scientific studies show fish oil omega-3 fatty acids offer significant protective benefit for prostate health.

Fish Oil Omega-3 Fatty Acids Offer the First Line of Defense Against Prostate Cancer

In contrast to this attack on omega-3s, the scientific literature overwhelmingly identifies diets high in omega-6 fats, trans-fatty acids, and saturated fats as associated with greater prostate cancer risk, whereas increased intake of long-chain omega-3 fats from fish has been shown to reduce risk. Based on consistent findings across a wide range of human populations, scientific research has identified why eating the wrong kinds of fatty acids provokes a stimulatory effect on prostate cancer.29,30

To ascertain what occurs after dietary fatty acids are consumed, the biochemical pathway for fatty acid metabolism provides the answers. For example, let us assume that for dinner, you eat a steak (a source of saturated fat, as well as arachidonic acid) and a salad, along with a typical salad dressing rich in linoleic acid, an omega-6 fat (e.g., safflower oil).

Arachidonic-Acid

Biochemically, omega-6 fat readily converts to arachidonic acid in the body. In response, the body attempts to compensate for excess arachidonic acid through the 5-lipoxygenase (5-LOX) pathway. Multiple studies strongly show that 5-LOX enzymatic by-products like leukotriene B4 and 5-HETE directly stimulate prostate cancer cell proliferation through several well-defined mechanisms.31-36

For example, arachidonic acid is metabolized by 5-LOX to 5-hydroxyeicosatetraenoic acid (5-HETE), a potent survival factor that prostate cancer cells use to escape destruction.37,38 Consuming a diet of foods rich in arachidonic acid, or precursors to arachidonic acid like the omega-6 fat linoleic acid, directly provokes the production of dangerous 5-LOX metabolic by-products, which can promote the progression of prostate cancer. In addition to 5-HETE, 5-LOX also metabolizes arachidonic acid into leukotriene B4, a potent pro-inflammatory agent that causes destructive reactions throughout the body and inflicts severe damage to the arterial wall.39-41

If arachidonic acid levels are reduced, a corresponding suppression of the 5-LOX products 5-HETE and leukotriene B4 will occur. A wealth of scientific research clearly demonstrates that supplementation with long-chain fatty acids like EPA and DHA from fish oil can help reduce the production of arachidonic acid-derived eicosanoids in the body.42

In contrast with the misinterpreted results presented in this report of men who were not consuming significant amounts of omega-3s, many other clinical studies indicate substantial benefit with omega-3 fatty acid intake in prostate cancer.

Additional Studies Indicate Substantial Benefit With Increased Intake of Omega-3 Fatty Acids

The report attacking omega-3s conflicts with prior studies demonstrating that increased intake of omega-3 fats has been shown to reduce prostate cancer risk and diets high in omega-6 fats are associated with greater risk. The analysis also suggests a relationship between increased omega-6 fatty acid levels and decreased risk of prostate cancer, which is, again, utterly inconsistent with the known pro-inflammatory effects of omega-6 fatty acids.

  • A 2010 meta-analysis found a 63% reduction in prostate cancer death rates in those with higher fish consumption.1
  • A 2004 study of 47 ,866 men found a trend toward decreased risk of prostate cancer with increasing levels of EPA and DHA.2
  • A 2007 Harvard study of 14, 916 men found lower incidence of prostate cancer in men who had higher levels of long chain omega-3 fatty acids.3
  • A 2013 Harvard study of 293, 464 men found increased omega-3 fatty acid intake was associated with significantly lower rate of fatal prostate cancer.4
  • A 2012 Harvard study of 525 men found a 40% lower prostate cancer death rate among men with the highest intake of marine fatty acids.5
  • A 2011 Duke University study found an increased omega-6:omega-3 ratio (i.e., more omega-6 and less omega-3) was associated with a significantly elevated risk of high grade prostate cancer.6
  • A 1999 New Zealand study found significantly lower rates of prostate cancer with higher blood levels of EPA and DHA.7
  • A 1999 Korean study found increased blood levels of omega-3 fatty acids associated with lower rates of prostate cancer and benign prostatic hyperplasia.8
  • A 2003 prospective study reported “that men with high consumption of fish had a lower risk of prostate cancer, especially for metastatic cancer.”10
  • A 2010 study that evaluated nutrient intake and prostate cancer risk concluded “High intake of omega-6 fatty acids, through their effects on inflammation and oxidative stress, may increase prostate cancer risk.”43
  • The University of Chicago conducted a study published in 2004 that showed PSA levels rose in tandem with the omega-6 to omega-3 ratio in Jamaican men whose PSA was >10 ng/mL. The researchers noted “Increased levels of Omega6 PUFAs and the ratio of Omega6/Omega3 PUFAs in Jamaican men are associated with an increased mean PSA level and risk of prostate cancer.”44
  • In addition to the clinical trial literature indicating consistent benefits with omega-3 fatty acid intake, traditional Japanese and Mediterranean diets rich in omega-3 fatty acids show a strong, consistent risk reduction in prostate cancer vs. Western diets rich in omega-6 and saturated fat.

Traditional Diets in Japan and The Mediterranean Region High in Fish are Protective Against Prostate Cancer

The results set forth by authors of the negative report on fish oil that omega-3 intake may be linked to prostate cancer are inconsistent, and in abject contrast, to longstanding evidence that diets high in marine lipids, such as the traditional Japanese diet and the Mediterranean diet, are protective against prostate cancer.

For example, the traditional Japanese diet, rich in omega-3 fatty acids from fish, confers protection against prostate cancer, as does the relatively high intake of fermented soy products and relatively low levels of saturated fat.45 The characteristics of the traditional Japanese diet high in soybean products, high in fish, and low in red meat are highly relevant in prostate cancer biology. In all likelihood, the traditional Japanese diet reduces the risk of prostate cancer through a combination of characteristics that generate a synergistic, anti-cancer effect (on prostate cancer).

Likewise, the protective properties of the Mediterranean diet in relation to heart disease and prostate cancer risk are well-established. Several aspects of this dietary pattern are protective, including regular consumption of small fish (smaller fish are less likely to contain contaminants than larger predatory fish such as tuna), high olive oil intake (there is synergy between olive polyphenols and fish oil), high daily ingestion of fresh vegetables, whole fruits (not pasteurized fruit juice rich in concentrated fructose), high-fiber cereals and legumes, and low intake of saturated animal fats and red meat.46

Benefit Clearly Outweighs Risk for Fish Oil Supplementation Among Men

Overwhelming evidence currently available strongly favors fish oil supplementation for most aging humans.

Fish oil and greater marine omega-3 intake have repeatedly and consistently been shown to reduce cardiovascular risk across multiple types of studies. For example:

A randomized, placebo-controlled trial found 1,800 mg of combined EPA plus DHA was associated with a 10%lower rate of cardiac events, 12% lower rate of non-fatal infarctions, and an almost 11% lower rate of cardiac deaths.47

In a large intervention study, 18,000 patients were randomized to receive either a statin medication alone or a statin plus 1,800 mg of EPA-fish oil daily. After five years, those with a history of coronary artery disease had a19% lower rate of major coronary events in the statin-plus EPA-fish oil group compared to the statin-only group.48

A randomized, double-blind, placebo-controlled trial with chronic hemodialysis patients found that 1,700 mg of omega-3 fatty acids daily was associated with a 70% reduction in the relative risk of myocardial infarction.49

A randomized, controlled trial using 3,300 mg of EPA and DHA (and then a decreased dosage) found a trend toward lower cardiovascular event occurrence with fish oil supplementation. Seven cardiovascular events occurred in the placebo group (not given fish oil) while only two cardiovascular events occurred in the fish oil-supplemented group during the study.50

A meta-analysis with an average fish oil dose of 3,700 mg found lowered systolic blood pressure by an average 2.1 mmHg and diastolic by 1.6 mmHg.51

In a randomized trial with peripheral arterial disease patients, 2,000 mg of omega-3 fatty acids daily resulted in a 49% improvement in flow-mediated dilation, a marker of endothelial cell health.52

The GISSI-Prevenzione study (a large, randomized, controlled trial) found that 1,000 mg/day of EPA and DHA in 11,323 patients with a history of recent myocardial infarction reduced the risk of total mortality by 20% andsudden death by 45%.53,54

The DART study — a randomized, controlled trial that examined the effects of advising 2,033 subjects to increase dietary fatty fish — revealed a 29% reduction in all-cause mortality compared with those not advised.55

A 2009 meta-analysis of randomized, controlled trials found that dietary supplementation with omega-3 fatty acids reduced the incidence of sudden cardiac death in subjects with prior myocardial infarction.56

Another 2009 meta-analysis of randomized, controlled trials found that dietary supplementation with omega-3 fatty acids reduced the risk of cardiovascular death, sudden cardiac death, all-cause mortality, and non-fatal cardiovascular events in patients with a history of certain cardiovascular events or risk factors.57

A 2008 meta-analysis found a significant reduction in death from cardiac causes with fish oil supplementation.58

A 2002 meta-analysis of randomized, controlled trials concluded that omega-3 fatty acids reduced overall mortality, mortality due to myocardial infarction, and sudden death in patients with coronary heart disease.59

Will this Flawed Report Prompt an Epidemic of Prostate Cancer?

Regrettably, the public is poorly served by relying on a sound-bite frenzied news media for health data, which often involves parading a provocative medical headline without a deep, thorough evaluation of the study’s validity.

This “science by ambush” denies an opportunity for meaningful rebuttal, since the media never wants to admit last week’s headline news story was bogus.

The average percentage difference (0.18%) of plasma long-chain omega-3 fatty acids from a single baseline test renders this study meaningless. The authors don’t even know if their study subjects were eating fish or taking fish oil supplements. We at Life Extension have criticized certain studies that solely rely on food questionnaires, but this attack on omega-3s didn’t even attempt to ascertain if study subjects were ingesting the nutrient (omega-3s) in question. Yet its authors presumptuously warn of potential risks in consuming supplemental omega-3s!

The lack of rigor, as well as multiple layers of methodological problems and errors, notwithstanding the complete lack of consistency with the known, well-established biology and biochemistry of prostate cancer should prompt outrage in the scientific and medical community.

The danger of this deeply flawed, compromised analysis is that aging men obtaining health information through the mainstream media will cease omega-3 fatty acid ingestion.

The consequences may be profound if aging men shun omega-3 fatty acid supplementation as a result of this flawed study and follows its implied recommendations to consume more omega-6 fats, which enhance inflammation and create a better environment for prostate cancer, as well as cardiovascular disease to flourish.

Although the researchers attempted to statistically model (through multivariate analysis) and control for some (but not all) critical, confounding risk factors like family history, the higher baseline PSA readings (implying more preexisting cancers) and positive family history (1st degree male relative with prostate cancer) in men who went on to develop prostate cancer raise concerns for the integrity of the analysis results. Along with these confounding factors, the marginal difference in baseline plasma omega-3 levels of men who later developed prostate cancer cannot rationally implicate omega-3s as having a causal or causative effect. The plasma omega-3 levels of the entire study group showed consumption of omega-3 from food was inadequate and intake of meaningful fish oil supplementation non-existent.

Educated health consumers should continue to ingest omega-3 fatty acids.

This report will be updated as more of Life Extension’s scientific advisors provide their input.

Written By: William Faloon, Luke Huber, ND, MBA, Kira Schmid, ND, Blake Gossard, Scott Fogle, ND

Article Source: http://www.lifeextension.com/Featured-Articles/2013/8/Fish-and-Prostate-Cancer-Risk-Fact-or-Fiction/Page-01

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