Low Testosterone Levels linked to increases in death – Boston Testosterone Partners

Leave a comment

Boston Testosterone Partners

Boston Testosterone Partners

Boston, Massachusetts – Beginning at age 30, men’s testosterone begins to drop and , on average, testosterone levels drop by 1% or more a year so by age fifty your testosterone levels may be 50% of what they were at age 30.  Low testosterone is also referred to as low androgens, andropause, testosterone deficiency or low T.

Some of the common symptoms of low testosterone often include low libido, mood changes, insomnia, fatigue, loss of muscle mass and strength, bone loss, and weight gain.

A report published in the British journal Heart reveals an increased risk of early death from all causes and cardiovascular disease among men who had low testosterone levels.

Researchers in that study analyzed data from 930 already sick  men with cardiovascular disease who underwent elective coronary angiography in a cardiac referral center between 2000 and 2002.  Total testosterone and bioavailable testosterone were measured on the day of their procedure.

The subjects were followed for about 7 years.  129 deaths occurred over the 930 men during that time.  73 of the deaths were due to their related cardiovascular disease.  24 percent of the participants had either low total or bioavailable testosterone.

Results:  21 percent of those with deficient bioavailable testosterone levels died from all causes over follow-up, compared to 12 percent of those with normal levels.

Low bioavailable testosterone levels were also associated with an increased risk of dying of cardiovascular causes.  Moreover, borderline low levels of total testosterone were associated with an increased risk of dying over follow-up.

“Clinical studies of testosterone supplementation in men with low testosterone are associated with reduced visceral adiposity, improved insulin sensitivity and an improved metabolic profile. Studies in subjects with cardiovascular diseases also suggested beneficial effects, with improved functional capacity in heart failure and improved symptoms in subjects with coronary artery disease.” says Dr Ronald C. W. Ma and Peter C. Y. Tong of Chinese University of Hong Kong and Prince of Wales Hospital, as part of the study.

“Compared with research on estrogens and cardiovascular disease, the role of androgens in the pathogenesis of metabolic and cardiovascular diseases has taken a backseat for many years,” they note. “Recent data suggest that this important pathway warrants a lot more attention.”



Testosterone Replacement Therapy with Boston Testosterone Partners, now available nationwide. We are New England’s leading choice for Male Wellness and Hormone Restoration for the treatment Low T, hypogonadism, Andropause and ED. Our medical director is a 25 year MD who has, for over ten years, been balancing both male and female hormones. He has been trained as a Hormone Specialist and has balanced well over a thousand male and female patients across the nation. Our patients have constant doctor interaction, he is always available daily to answer questions for our patients.

Our protocols include Sermorelin-GHRP2 Therapy, Glutathione Therapy, numerous Amino Acid Injectable combinations, personally tailored Weight Loss injectables, Cialis or Viagra sublinguals, Oxytocin sprays, and more..

Our services also include proven medical weight loss systems for BOTH men and women utilizing a proprietary combination of B12, B3, MIC, Amino Acids and L-Carnitine specially compounded for our patients. We offer uniquely compounded SuperB and LipoC injectables and capsules, available only from our compounding pharmacy.


Do you know what your Testosterone Level is?

1 Comment

At Boston Testosterone Partners, we can help!

Info@BostonTestosterone.com or

855-617-MEDS (6337)

Boston Testosterone Partners

Boston Testosterone Partners

It used to be that men could blame their lack of energy and decreasing libido on getting older. But not any more. If you’re a man age 50 or older who is tired for apparently no reason or has diminished sex drive, there’s a good chance that your levels of the hormone testosterone are lower than normal — and you could benefit from testosterone therapy.

Until recently, many doctors didn’t fully understand the importance of enough testosterone. But now, most physicians are aware that low testosterone (also called “low T”) has many negative effects that go well beyond reduced energy and libido.

Getting a testosterone test is easy and inexpensive. If your T levels are low, testosterone treatments are highly effective at relieving specific symptoms and improving overall health.


Giving testosterone to men with low T has been shown to…

Improve libido by acting on T receptors in brain regions associated with sexual desire.

Improve erection quality by activating T receptors in the penis. In one study, 60% of men on T therapy reported improved erections.

Boost energy. Men report an increased sense of drive and well-being.

Improve body composition by increasing muscle mass and reducing body fat. In one study, men who used T gel, a testosterone treatment, for six months and did not exercise or change diet, added an average 4.4 pounds in muscle and lost 1.75 pounds of fat.

Increase bone density. Studies show that men with low T are at increased risk for bone fractures and that bone density improves measurably in men with low T who get testosterone therapy.

Prevent disease. Normal T levels reduce the risk for diabetes and coronary artery disease.

Increase longevity. Studies show that men with normal T levels live longer, on average, than men with low T.

Testosterone therapy is safe for most men. For decades, it was believed that increasing testosterone made prostate tumors grow. That’s recently been disproven, in part by research that I’ve conducted personally. If you have low T and no signs of prostate cancer, such as an elevated prostate-specific antigen (PSA) level or enlarged prostate, the data suggests that there’s no risk in testosterone therapy. Even men with abnormal PSA levels may receive testosterone therapy if a biopsy is negative. I also offer testosterone treatment to men with low testosterone after they have been successfully treated for prostate cancer.


In my opinion, all men age 50 and older should have their testosterone level screened as part of their annual physical exams. I also recommend screening when men have significantly reduced sex drive… low energy for no apparent reason… difficulty achieving or maintaining an erection… decreased muscle mass and/or increased body fat, especially around the midsection (declining testosterone may play a role in the normal changes that come with aging)… loss of height (a sign of tiny fractures in the vertebrae due to osteoporosis)… increased irritability… and/or lack of motivation.

Important: Be sure to ask for both testosterone blood tests…

Total testosterone is the standard test that’s been used for decades. It will indicate if your total testosterone is subnormal (less than 350 nanograms/dL). But it does not indicate the amount of testosterone available to the body. That’s why it’s important to also get a second test.

The analog free T test is the most common and reliable test to measure free testosterone, the amount of testosterone that is in the bloodstream and biologically available (not bound to any carrier proteins). A level less than 1.5 picograms/dL indicates that you have low T and could benefit from testosterone therapy.

Note: The tests are not affected by diet, exercise or sexual activity prior to having blood drawn.


If you have low T, there are several effective treatments that can be administered by your primary care doctor or by a urologist…

Testosterone gel (AndroGel, Testim) is the most widely used treatment, and the one I prescribe first. The usual starting dose is five grams, rubbed into the upper arms and shoulders once a day. It takes about two hours for the gel to be absorbed, during which time men should avoid skin-to-skin contact with others.

The gel is completely absorbed, but the amount of testosterone that actually enters the bloodstream varies from person to person, so you must have your T levels checked a few weeks after starting treatment so the dosage can be adjusted if necessary. If this test still shows low T, upping the dosage or switching brands can often help. Gel therapy costs about $300 per month. Insurance may cover the cost, depending on the state you live in.

Injections. Some men don’t absorb testosterone from the gel even in high doses. In these cases, I usually prescribe testosterone injections — typically 200 milligrams every two weeks. They’re usually injected in the buttocks by a physician, although men can learn to self-inject into their thighs. While injections aren’t as convenient as gel, they’re less expensive — about $5 per shot. A longer-acting injection called Nebido, which lasts 10 weeks, is currently under review by the FDA.

Pellets. Extended-release testosterone pellets are a relatively new option. Six to eight pellets, each the size of a rice grain, are inserted under the skin of the buttocks (a painless procedure using a local anesthetic and done in the doctor’s office). They are gradually absorbed into the body and maintain T levels for three to six months. Pellets are a good option for men who don’t like applying gel daily. Cost is about $500 for a three- to six-month application and is usually covered by insurance.

Once you begin testosterone therapy, it may take a month or two for T levels to rise to the point where you experience noticeable benefits. As long as they continue to benefit, most men can stay on the therapy for many years.

Source: Abraham Morgentaler, MD, associate clinical professor of urology at Harvard Medical School, Boston.  He is author of several books, including Testosterone for Life (McGraw-Hill).

Testosterone Replacement Therapy Doctors

Boston Testosterone Partners

Finger Length and The Casanova Pattern – Boston Testosterone Partners

1 Comment

It’s a simple do-it-yourself health test, no equipment needed: Stretch your hands out in front of you and look at how long your fingers are. Most men have ring fingers that are slightly longer than their index fingers, while in most women these fingers are roughly the same length.

So what? Well, variations to these typical findings may have important implications for your health. It turns out that hormones released in the womb influence finger length and, as odd as it sounds, they also have important effects on future health and behavior. Gad Saad, PhD, professor of marketing and research chair in evolutionary behavioral sciences and Darwinian consumption at Concordia University in Montreal, and his colleagues have examined numerous studies involving finger length and found lots of interesting associations.


Dr. Saad refers to finger length as “a proxy of prenatal testosterone exposure,” explaining that the ratio between the index and the ring finger is determined early in pregnancy. The more exposure the fetus has to this predominantly male hormone, the more so-called masculine traits the adult will have (whether male or female) and the longer the ring finger will be.

Interesting fact:Having a long ring finger is known as the “Casanova pattern,” since Casanova was notably reputed to have a very long ring finger (in relation to his index finger). Dr. Saad told me that this means that “he had a highly masculinized digit ratio.”

According to Dr. Saad, early exposure to testosterone also affects how organs are formed, which is why this ratio is relevant to your future susceptibility to disease. In most people, the discrepancy between the ring and index finger is more pronounced on the right hand than the left.


Here are some of the conclusions scientists have reached in recent years…

  • An impact on disease risk. In the British Journal of Cancer, researchers reported that men whose index fingers were longer than their ring fingers (indicating less prenatal exposure to testosterone) were at lower risk for prostate cancer. On the other hand, scientists at Liverpool University observed that males with longer index fingers were at a higher risk for heart attack than other males, presumably because testosterone is heart-protective.
  • A clue to sexuality. The Casanova pattern may offer a clue to sexual orientation. UC Berkeley scientists found that lesbian women tended (like men) to have longer ring fingers than index fingers. But, Dr. Saad said, the findings aren’t so straightforward for gay men. In homosexuals with several older, heterosexual brothers, researchers found a tendency to have much longer ring fingers than straight men… while those without older brothers were more likely to have the same male-pattern, longer ring finger as straight men.
  • More sports ability. Scientists believe that high testosterone translates into better success on the playing field, as it encourages aggression, competitiveness and dominant behavior and also facilitates power, endurance and visual-spatial skills. At Temple University, investigators noted that men with longer ring fingers tended to do better in sports such as football and soccer.
  • More aggression and risk-taking. At Cambridge University in England, researchers found that financial traders with longer ring fingers tended to be more aggressive and earned the most money. In another study, an analysis of students at Concordia, Dr. Saad and his team discovered that males with longer ring fingers took more recreational, social and financial risks.


Your finger length is far from a perfect predictor of your health, of course, but you can consider it a helpful clue to what health challenges the future may hold — so you do all you can to circumvent them. For instance, if you are a male and your finger ratio suggests increased cardiovascular risk, ask your doctor to assess your heart health and pay close attention to cardio-related lifestyle choices such as diet and exercise. Plus, it’s a great conversation-starter when you need to make small talk — and that can be plenty helpful in life, too!

Source: Gad Saad, PhD, professor of marketing, holder of the Concordia University Research Chair in Evolutionary Behavioral Sciences and Darwinian Consumption, John Molson School of Business, Concordia University, Montreal, Quebec, Canada. Dr. Saad is author of The Evolutionary Bases of Consumption (Psychology Press) and the upcoming The Consuming Instinct: What Juicy Burgers, Ferraris, Pornography, and Gift Giving Reveal About Human Nature (Prometheus Books, to be published June 2011). He is a blogger at Psychology Today (www.PsychologyToday.com/blog/homo-consumericus).


Testosterone Replacement Therapy with Boston Testosterone Partners, now available nationwide. We are New England’s leading choice for Male Wellness and Hormone Restoration for the treatment Low T, hypogonadism, Andropause and ED. Our medical director is a 25 year MD who has, for over ten years, been balancing both male and female hormones. He has been trained as a Hormone Specialist and has balanced well over a thousand male and female patients across the nation. Our patients have constant doctor interaction, he is always available daily to answer questions for our patients.

Our protocols include Sermorelin-GHRP2 Therapy, Glutathione Therapy, numerous Amino Acid Injectable combinations, personally tailored Weight Loss injectables, Cialis or Viagra sublinguals, Oxytocin sprays, and more..

Our services also include proven medical weight loss systems for BOTH men and women utilizing a proprietary combination of B12, B3, MIC, Amino Acids and L-Carnitine specially compounded for our patients. We offer uniquely compounded SuperB and LipoC injectables and capsules, available only from our compounding pharmacy.


Fish and Prostate Cancer Risk: Fact or Fiction

Leave a comment

Boston Testosterone Partners
Boston, Massachusetts
Testosterone and Hormone Replacement Therapy Doctors
Testosterone Replacement Therapy Doctors

Boston Testosterone Partners

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

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 themulti-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 plasma omega-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 theiromega-3 consumption through diet and supplements.

Also absent from the reporting was that more men with slightly higher omega-3 plasma levels hadconfounding 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 miniscule 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 as omega-3swere 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 purified fish 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.17 We 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 tobone 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 diseaseto 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-3percentage 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 ofcruciferous 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 of cold-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 higheromega-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 only4.66%.

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 a43% to 71% increase in prostate cancer incidence. Dedicated fish oil supplement users, on the other hand have over100% 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 salmonthe 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.

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).


Biochemically, saturated fat and linoleic acid, a type of omega-6 fat, readily convert 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 plus1,800 mg of EPA-fish oil daily. After five years, those with a history of coronary artery disease had a 19% 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 11,323patients with a history of recent myocardial infarction reduced the risk of total mortality by 20% and sudden deathby 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.


  1. Szymanski KM, Wheeler DC, Mucci LA. Fish consumption and prostate cancer risk: a review and meta-analysis. The American journal of clinical nutrition. Nov 2010;92(5):1223-1233.
  2. Leitzmann MF, Stampfer MJ, Michaud DS, et al. Dietary intake of n-3 and n-6 fatty acids and the risk of prostate cancer. The American journal of clinical nutrition. Jul 2004;80(1):204-216.
  3. Chavarro JE, Stampfer MJ, Li H, Campos H, Kurth T, Ma J. A prospective study of polyunsaturated fatty acid levels in blood and prostate cancer risk. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. Jul 2007;16(7):1364-1370.
  4. Bosire C, Stampfer MJ, Subar AF, et al. Index-based dietary patterns and the risk of prostate cancer in the NIH-AARP diet and health study. American journal of epidemiology. Mar 15 2013;177(6):504-513.
  5. Epstein MM, Kasperzyk JL, Mucci LA, et al. Dietary fatty acid intake and prostate cancer survival in Orebro County, Sweden. American journal of epidemiology. Aug 1 2012;176(3):240-252.
  6. Williams CD, Whitley BM, Hoyo C, et al. A high ratio of dietary n-6/n-3 polyunsaturated fatty acids is associated with increased risk of prostate cancer. Nutrition research (New York, N.Y.). Jan 2011;31(1):1-8.
  7. Norrish AE, Skeaff CM, Arribas GL, Sharpe SJ, Jackson RT. Prostate cancer risk and consumption of fish oils: a dietary biomarker-based case-control study. British journal of cancer. Dec 1999;81(7):1238-1242.
  8. Yang YJ, Lee SH, Hong SJ, Chung BC. Comparison of fatty acid profiles in the serum of patients with prostate cancer and benign prostatic hyperplasia. Clinical biochemistry. Aug 1999;32(6):405-409.
  9. Astorg P. Dietary N-6 and N-3 polyunsaturated fatty acids and prostate cancer risk: a review of epidemiological and experimental evidence. Cancer causes & control : CCC. May 2004;15(4):367-386.
  10. Augustsson K, Michaud DS, Rimm EB, et al. A prospective study of intake of fish and marine fatty acids and prostate cancer. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. Jan 2003;12(1):64-67.
  11. Aronson WJ, Kobayashi N, Barnard RJ, et al. Phase II prospective randomized trial of a low-fat diet with fish oil supplementation in men undergoing radical prostatectomy. Cancer prevention research (Philadelphia, Pa.). Dec 2011;4(12):2062-2071.
  12. Brasky TM, Darke AK, Song X, et al. Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial.Journal of the National Cancer Institute. Jul 10 2013.
  13. Cao J, Schwichtenberg KA, Hanson NQ, Tsai MY. Incorporation and clearance of omega-3 fatty acids in erythrocyte membranes and plasma phospholipids. Clinical chemistry. Dec 2006;52(12):2265-2272.
  14. Harris W. et al. Comparative effects of an acute dose of fish oil on omega-3 fatty acid levels in red blood cells versus plasma: Implications for clinical utility. Journal of Clinical Lipidology, 5/9/2013.
  15. American Cancer Society. Available at: http://www.cancer.org/cancer/prostatecancer/detailedguide/prostate-cancer-risk-factors . Accessed 7/15/2013.
  16. University of Maryland Medical Center. Prostate cancer. Available at:http://umm.edu/health/medical/altmed/condition/prostate-cancer Accessed 7/15/2013.
  17. Thomas JA, 2nd, Gerber L, Banez LL, et al. Prostate cancer risk in men with baseline history of coronary artery disease: results from the REDUCE Study. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. Apr 2012;21(4):576-581.
  18. Farhat G. et al. The link between osteoporosis and cardiovascular disease. Clin Cases Miner Bone Metab. 2008 Jan-Apr; 5(1): 19–34.
  19. Bruner DW, Moore D, Parlanti A, Dorgan J, Engstrom P. Relative risk of prostate cancer for men with affected relatives: systematic review and meta-analysis. International journal of cancer. Journal international du cancer. Dec 10 2003;107(5):797-803.
  20. Chinni SR, Li Y, Upadhyay S, Koppolu PK, Sarkar FH. Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells. Oncogene. May 24 2001;20(23):2927-2936.
  21. Cohen JH, Kristal AR, Stanford JL. Fruit and vegetable intakes and prostate cancer risk. Journal of the National Cancer Institute. Jan 5 2000;92(1):61-68.
  22. Morgentaler A. Testosterone For Life. New York, NY: McGraw-Hill; 2008.
  23. Vijayakumar S, Mehta RR, Boerner PS, Packianathan S, Mehta RG. Clinical trials involving vitamin D analogs in prostate cancer. Cancer journal (Sudbury, Mass.). Sep-Oct 2005;11(5):362-373.
  24. Lou YR, Qiao S, Talonpoika R, Syvala H, Tuohimaa P. The role of Vitamin D3 metabolism in prostate cancer. The Journal of steroid biochemistry and molecular biology. Nov 2004;92(4):317-325.
  25. John EM, Schwartz GG, Koo J, Van Den Berg D, Ingles SA. Sun exposure, vitamin D receptor gene polymorphisms, and risk of advanced prostate cancer. Cancer research. Jun 15 2005;65(12):5470-5479.
  26. Ben Sahra I, Laurent K, Giuliano S, et al. Targeting cancer cell metabolism: the combination of metformin and 2-deoxyglucose induces p53-dependent apoptosis in prostate cancer cells. Cancer research. Mar 15 2010;70(6):2465-2475.
  27. Teiten MH, Gaascht F, Eifes S, Dicato M, Diederich M. Chemopreventive potential of curcumin in prostate cancer.Genes & nutrition. Mar 2010;5(1):61-74.
  28. Piantino CB, Salvadori FA, Ayres PP, et al. An evaluation of the anti-neoplastic activity of curcumin in prostate cancer cell lines. International braz j urol : official journal of the Brazilian Society of Urology. May-Jun 2009;35(3):354-360; discussion 361.
  29. Newcomer LM, King IB, Wicklund KG, Stanford JL. The association of fatty acids with prostate cancer risk. The Prostate. Jun 1 2001;47(4):262-268.
  30. Niclis C, Diaz Mdel P, Eynard AR, Roman MD, La Vecchia C. Dietary habits and prostate cancer prevention: a review of observational studies by focusing on South America. Nutrition and cancer. 2012;64(1):23-33.
  31. Hassan S, Carraway RE. Involvement of arachidonic acid metabolism and EGF receptor in neurotensin-induced prostate cancer PC3 cell growth. Regulatory peptides. Jan 15 2006;133(1-3):105-114.
  32. Moretti RM, Montagnani Marelli M, Sala A, Motta M, Limonta P. Activation of the orphan nuclear receptor RORalpha counteracts the proliferative effect of fatty acids on prostate cancer cells: crucial role of 5-lipoxygenase.International journal of cancer. Journal international du cancer. Oct 20 2004;112(1):87-93.
  33. Matsuyama M, Yoshimura R, Mitsuhashi M, et al. Expression of lipoxygenase in human prostate cancer and growth reduction by its inhibitors. International journal of oncology. Apr 2004;24(4):821-827.
  34. Gupta S, Srivastava M, Ahmad N, Sakamoto K, Bostwick DG, Mukhtar H. Lipoxygenase-5 is overexpressed in prostate adenocarcinoma. Cancer. Feb 15 2001;91(4):737-743.
  35. Ghosh J, Myers CE. Arachidonic acid stimulates prostate cancer cell growth: critical role of 5-lipoxygenase.Biochemical and biophysical research communications. Jun 18 1997;235(2):418-423.
  36. Gao X, Grignon DJ, Chbihi T, et al. Elevated 12-lipoxygenase mRNA expression correlates with advanced stage and poor differentiation of human prostate cancer. Urology. Aug 1995;46(2):227-237.
  37. Sundaram S, Ghosh J. Expression of 5-oxoETE receptor in prostate cancer cells: critical role in survival. Biochemical and biophysical research communications. Jan 6 2006;339(1):93-98.
  38. Myers CE, Ghosh J. Lipoxygenase inhibition in prostate cancer. European urology. 1999;35(5-6):395-398.
  39. Helgadottir A, Manolescu A, Thorleifsson G, et al. The gene encoding 5-lipoxygenase activating protein confers risk of myocardial infarction and stroke. Nature genetics. Mar 2004;36(3):233-239.
  40. Poff CD, Balazy M. Drugs that target lipoxygenases and leukotrienes as emerging therapies for asthma and cancer.Current drug targets. Inflammation and allergy. Mar 2004;3(1):19-33.
  41. Crooks SW, Bayley DL, Hill SL, Stockley RA. Bronchial inflammation in acute bacterial exacerbations of chronic bronchitis: the role of leukotriene B4. The European respiratory journal. Feb 2000;15(2):274-280.
  42. Adam O, Beringer C, Kless T, et al. Anti-inflammatory effects of a low arachidonic acid diet and fish oil in patients with rheumatoid arthritis. Rheumatology international. Jan 2003;23(1):27-36.
  43. Kristal AR, Arnold KB, Neuhouser ML, et al. Diet, supplement use, and prostate cancer risk: results from the prostate cancer prevention trial. American journal of epidemiology. Sep 1 2010;172(5):566-577.
  44. Ritch CR, Brendler CB, Wan RL, Pickett KE, Sokoloff MH. Relationship of erythrocyte membrane polyunsaturated fatty acids and prostate-specific antigen levels in Jamaican men. BJU international. Jun 2004;93(9):1211-1215.
  45. Mori M, Masumori N, Fukuta F, et al. Traditional Japanese diet and prostate cancer. Molecular nutrition & food research. Feb 2009;53(2):191-200.
  46. Ferris-Tortajada J, Berbel-Tornero O, Garcia-Castell J, Ortega-Garcia JA, Lopez-Andreu JA. [Dietetic factors associated with prostate cancer: protective effects of Mediterranean diet]. Actas urologicas espanolas. Apr 2012;36(4):239-245.
  47. Singh RB, Niaz MA, Sharma JP, Kumar R, Rastogi V, Moshiri M. Randomized, double-blind, placebo-controlled trial of fish oil and mustard oil in patients with suspected acute myocardial infarction: the Indian experiment of infarct survival–4. Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy. Jul 1997;11(3):485-491.
  48. Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet. Mar 31 2007;369(9567):1090-1098.
  49. Svensson M, Schmidt EB, Jorgensen KA, Christensen JH. N-3 fatty acids as secondary prevention against cardiovascular events in patients who undergo chronic hemodialysis: a randomized, placebo-controlled intervention trial. Clinical journal of the American Society of Nephrology : CJASN. Jul 2006;1(4):780-786.
  50. von Schacky C, Angerer P, Kothny W, Theisen K, Mudra H. The effect of dietary omega-3 fatty acids on coronary atherosclerosis. A randomized, double-blind, placebo-controlled trial. Annals of internal medicine. Apr 6 1999;130(7):554-562.
  51. Geleijnse JM, Giltay EJ, Grobbee DE, Donders AR, Kok FJ. Blood pressure response to fish oil supplementation: metaregression analysis of randomized trials. Journal of hypertension. Aug 2002;20(8):1493-1499.
  52. Schiano V, Laurenzano E, Brevetti G, et al. Omega-3 polyunsaturated fatty acid in peripheral arterial disease: effect on lipid pattern, disease severity, inflammation profile, and endothelial function. Clinical nutrition (Edinburgh, Scotland). Apr 2008;27(2):241-247.
  53. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione. Circulation. Apr 23 2002;105(16):1897-1903.
  54. Efficacy of n-3 polyunsaturated fatty acids and feasibility of optimizing preventive strategies in patients at high cardiovascular risk: rationale, design and baseline characteristics of the Rischio and Prevenzione study, a large randomised trial in general practice. Trials. 2010;11:68.
  55. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet. Sep 30 1989;2(8666):757-761.
  56. Zhao YT, Chen Q, Sun YX, et al. Prevention of sudden cardiac death with omega-3 fatty acids in patients with coronary heart disease: a meta-analysis of randomized controlled trials. Annals of medicine. 2009;41(4):301-310.
  57. Marik PE, Varon J. Omega-3 dietary supplements and the risk of cardiovascular events: a systematic review.Clinical cardiology. Jul 2009;32(7):365-372.
  58. Leon H, Shibata MC, Sivakumaran S, Dorgan M, Chatterley T, Tsuyuki RT. Effect of fish oil on arrhythmias and mortality: systematic review. BMJ (Clinical research ed.). 2008;337:a2931.
  59. Bucher HC, Hengstler P, Schindler C, Meier G. N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials. The American journal of medicine. Mar 2002;112(4):298-304.

Why Testosterone Replacement Therapy (TRT) for Men should include adjunct therapies with PDE5 inhibitors – tadalafil (Cialis) and Sildenafil (Viagra).

Leave a comment

Boston, Massachusetts – Testosterone Replacement Therapy (TRT) for Men with adjunct therapies in PDE5 inhibitors such as tadalafil (Cialis) and Sildenafil (Viagra).  Here is another reason why many Boston Testosterone Partners patients love to include tadalafil troches into their therapy protocols.  They help men LOSE FAT.

Researchers from the University of Bonn treated mice with Viagra and made an amazing discovery: The drug converts undesirable white fat cells and could thus potentially melt the unwelcome “spare tire” around the midriff. In addition, the substance also decreases the risk of other complications caused by obesity. The results are now published in “The Journal of the Federation of American Societies for Experimental Biology” (FASEB).

59d74d68da5b538c1c0a2854b0cff762In addition to Testosterone Therapy, Sildenafil – better known as Viagra – is used to treat erectile dysfunction. This substance prevents degradation of cyclic guanosine mono-phosphate (cGMP), which then ensures blood supply for an erection. However, another effect of Viagra has been noticed quite some time ago – mice given sildenafil over longer periods of time were resistant to obesity when fed with high-fat diet. However, the cause for this reduced weight gain had been unclear. Researchers from the University of Bonn have been able to shed some light on this sildenafil effect. “We have been researching the effect of cGMP on fat cells for quite some time now,” reports Prof. Dr. Alexander Pfeifer, Director of the Institute for Pharmacology and Toxicology at the University of Bonn. “This is why sildenafil was a potentially interesting candidate for us.”

Viagra converts undesirable white fat cells into beige ones.  

Together with the PharmaCenter of the University of Bonn, the German Federal Institute for Drugs and Medical Devices (BfArM), and the Max Planck Institute for Heart and Lung Research, the team around Prof. Pfeifer studied the effect of sildenafil on fat cells in mice. The researchers administered the potency drug to the rodents for seven days. “The effects were quite amazing,” says Dr. Ana Kilic, one of Prof. Pfeifer’s colleagues. Sildenafil increased the conversion of white fat cells, which are found in human ‘problem areas’, into beige ones in the animals. “Beige fat cells burn the energy from ingested food and convert it to heat, says Prof. Pfeifer. Because the beige fat cells can “melt the fat” and thus fight obesity, researchers are very hopeful for their potential.

Positive effect on inflammation responses

In addition, the researchers observed something else of interest. If white fat cells are further “stuffed”/accumulating lipids, they are increasing in size and can synthesize and release hormones which in turn cause inflammation thus increasing the persons risk for chronic diseases. Such inflammatory responses may then lead to, e.g., cardio-vascular diseases resulting in heart attacks and strokes, as well as cancer and diabetes. “It seems that sildenafil prevented the fat cells in these mice from getting onto that slippery slope,” reports Prof. Pfeifer. Overall, the development of white cells seems to be healthier.

More than half a billion overweight people worldwide

Globally, over half a billion people are overweight. Present study has resulted in interesting starting points for further research on this mechanism. “Sildenafil is not only able to minimize erectile problems, but it can also reduce the risks of gaining excessive weight,” says Prof. Pfeifer. The researchers may have found a mechanism that allows converting the undesirable white fat cells into the “good” beige (brown-like) fat cells that “melt” away excess pounds. In addition, it might be possible to decrease complications related with obesity. “But this will need to be proven in additional studies,” adds Dr. Kilic.

Testosterone Replacement Therapy with Boston Testosterone Partners, now available nationwide. We are New England’s leading choice for Male Wellness and Hormone Restoration for the treatment Low T, hypogonadism, Andropause and ED. Our medical director is a 25 year MD who has, for over ten years, been balancing both male and female hormones. He has been trained as a Hormone Specialist and has balanced well over a thousand male and female patients across the nation. Our patients have constant doctor interaction, he is always available daily to answer questions for our patients.

Our protocols include Sermorelin-GHRP2 Therapy, Glutathione Therapy, numerous Amino Acid Injectable combinations, personally tailored Weight Loss injectables, Cialis or Viagra sublinguals, Oxytocin sprays, and more..

Our services also include proven medical weight loss systems for BOTH men and women utilizing a proprietary combination of B12, B3, MIC, Amino Acids and L-Carnitine specially compounded for our patients. We offer uniquely compounded SuperB and LipoC injectables and capsules, available only from our compounding pharmacy.




Oxytocin therapy now available at Boston Testosterone

Leave a comment

Boston Testosterone Partners

Boston Testosterone Partners

Boston Testosterone Partners

Boston, Massachusetts – Find out about the amazing benefits of Oxytocin Therapy at Boston Testosterone Partners.

Oxytocin – the natural way to enhance orgasm in men and women

Known as a desire hormone, the hormone oxytocin is naturally produced in our body and released at key moments – namely when we’re intimate with others. By supplementing this life-enriching hormone, greater orgasm can be achieved far more easily in men and women. Not only this, but oxytocin works to promote a generally improved sense of wellbeing and acts to reduce stress.

The full benefits of oxytocin are only now becoming apparent. It’s involved in the pleasure aspect of sex and is now believed by experts to actually cause orgasm. Studies have found that by supplementing the hormone oxytocin, multiple orgasms can be achieved in women and increased feelings of intimacy can be experienced by both sexes.

Oxytocin hormone supplement the closest thing to a Love Drug

The Oxytocin drug is a safe and potent supplement based on the naturally occurring hormone Oxytocin. It has far reaching benefits for the body and mind, including the ability to enhance orgasm experiences. Oxytocin for men assists emotional bonding as well as desire, and an Oxytocin orgasm for women is especially enhanced.

The hormone Oxytocin is probably best known for its role in childbirth and breastfeeding, although research has established that the Oxytocin drug can help forge deep connections with our partners, our children, our friends and even our pets. Excitingly, the Oxytocin orgasm is powerful for both men and women. It’s been shown to enhance orgasm – and induce multiple orgasms in women.

Oxytocin however, is more than merely a male or female orgasm enhancer. It plays many roles for men, and in women is an essential hormone released throughout their lives in certain conditions and scenarios.

How Oxytocin Hormone is Naturally Released in Body

Oxytocin is produced by the hypothalamus – the almond sized region of the brain located close to the brain stem that links the nervous system to the endocrine system via the pituitary gland. It’s released either via the pituitary gland straight into the bloodstream or to other parts of the brain and the spinal cord.

In childbirth, Oxytocin plays a vital role in triggering and regulating uterine contractions. If the contractions aren’t substantial enough, in a lot of cases Oxytocin is administered to help stimulate these contractions. Not only does this have a physical effect, but Oxytocin is a known as a ‘bonding hormone’ – ensuring that the mother starts to care for her young the moment after giving birth. The emotional and maternal reaction is heightened by the hormone, and the effects establish a bond between mother and baby.

Oxytocin also features in breast feeding. By helping the mother to relax, it allows milk to flow to feed her baby. Through this, scientists and doctors started to take note, as the relaxing and wellbeing effects became apparent.

Research also revealed that Oxytocin plays a huge role in the non-procreative aspects of sex. Both women and men release the Oxytocin hormone during lovemaking – and not only during orgasm. It also appears to be responsible for causing orgasms in the first place.

The Effects of the Hormone Oxytocin in Love Making

At our body’s normal level of production, Oxytocin encourages a mild desire to be kissed and cuddled by your lover. In fact being touched anywhere on the body leads to a rise in Oxytocin levels. This causes a chain reaction within the body, including the release of endorphins and testosterone, which results in both biological and psychological arousal.

Erogenous zones including earlobes, neck and genitals become sensitized to the effect of the hormone, and the body and mind become receptive and proactive in sexual activity. It not only arouses blood and the senses, but also promotes a bond of intimacy and closeness. The cycle continues to fire these pleasure giving endorphins and hormones and we naturally produce more Oxytocin and feel more pleasure as a reward.

By stimulating genital areas and causing the nerves to fire spontaneously, orgasm is reached far easier and more powerfully. In orgasm, male Oxytocin levels quintuple, while women need higher levels if they are to reach orgasm. And during peak sexual arousal, the Oxytocin levels become very high indeed. At this point multiple orgasms can occur.

Oxytocin’s further health and well being benefits

Using Oxytocin can also help regulate sleep patterns, and have a calming effect. Research is ongoing but observation seems to cite Oxytocin’s health giving benefits lying in its ability to counteract stress and the effects of the stress hormone cortisol. Nearly every disease and condition is aggravated by stress; anything that can help counteract the stress is therefore useful.

Oxytocin has a clear physical and emotional power. Not only does the hormone increase orgasm in men and women, it has the natural ability to generate meaningful bonds, calm and in turn increase personal wellbeing.

Prescription Oxytocin nasal spray

We are excited to announce that Oxytocin Nasal Spray is BTP’s latest addition to its comprehensive range of BIO-IDENTICAL HORMONE and TESTOSTERONE REPLACEMENT THERAPY.

Oxytocin is released via the pituitary hormone and it has been clinically proven to have a number of beneficial effects.  Oxytocin is being used for mood swings (depression), drug addition, autism, anxiety, schizophrenia, pain (particularly for fibromyalgia) and even as an aid to weight loss, (principally through appetite reduction); but perhaps oxytocin’s most highlighted use has been to help couples enjoy a closer (bonding/ loving) relationships and for individuals, (in particular for women- which in this case is unusual) to have more intense orgasms.

Testosterone Replacement Therapy Doctors

Boston Testosterone Partners

The world’s expert talks about this calming hormone

An Interview with Kerstin Uväs-Moberg, M.D., Ph. D

If you suffer from stress, high blood pressure, elevated cortisol in the blood, or other stress-related symptoms, you will be interested in oxytocin—a hormone which Dr. Kerstin Uväs-Moberg calls the calm and connection hormone.

How can you bring greater calm and connection into your life and the life of your children?

Kerstin Uväs-Moberg, M.D., Ph. D, author of The Oxytocin Factor, is a recognized world authority on oxytocin.  Her research took place at the famed Karolinska Institute in Stockholm and at the Swedish University of Agricultural Sciences in Uppsala, where she is Professor of Physiology.  Influential in obstetrics, psychology, pediatrics, child development, physical therapy and other fields, Dr. Uväs-Moberg has authored over four hundred scientific papers and lectures widely in Europe and the USA.

1. In your book, you state, “There are many scientific conferences on the topics of stress and pain, but very few conferences deal with calm, rest, and wellbeing.”  What does oxytocin have to do with calm, rest, and wellbeing?

Dr. Uväs-Moberg: Oxytocin, which was first noticed during birth labor and in nursing

mothers in 1906, acts as both a hormone and a neuropeptide.  It triggers a complex series of reactions that enhance your body’s relaxation and calmness. This is important in two ways.  The first (1) is the immediate health benefit of lowering stress-related symptoms and the second (2) is that repeated dosages of oxytocin seem to convert the immediate benefit into a long-lasting effect.  In our studies, animals who received as little as one dose per day for 5 days needed little additional oxytocin to stay calm for up to 3 weeks.  This suggests that oxytocin can offer stressed human beings a way to open up new pathways, to help them relax and restore calm immediately and across long term situations.  I stress oxytocin’s ability to grow or develop people’s relaxation and restoration capacity.

2. What is the relationship between oxytocin and adrenaline or other fight/flight responses?

Dr. Uväs-Moberg: The body is intelligent.  Oxytocin does have the reverse effects to flight or fight hormones, but the body doesn’t call on oxytocin in every situation.  Sometimes we are threatened or in danger and we must respond to our flight or fight hormones to protect ourselves.  However, oxytocin may even be able to serve us in potentially threatening situations.  For example, if we can stay calm in a tense situation, we may know enough to move away from danger. We can learn to avoid a fight and respond differently.


3. What does oxytocin actually do?

Dr. Uväs-Moberg: Oxytocin does two important things:  (1) lowers blood pressure and other stress-related responses, and (2) increases positive social behaviors, such as friendliness and desire to connect.  Oxytocin impacts the body in two ways.  The first is that it is a hormone released from the blood stream as it circulates in the body.  And, it is also released by the nerve centers inside the brain.  This means that it capable of having a direct impact because it is not only a blood born hormone.


Today, in my opinion, our relaxation responses are under-developed and we are much more stressed than we have been historically.  Therefore, everything that we can do to enhance our levels of oxytocin increases our options for wellbeing.  The results of an interesting longitudinal study between mothers and children demonstrate that real contact (eye contact and direct conversation) between mothers and children has been reduced by half. Mothers and their children are spending time in the same room, but only about half that time is spent in real contact.  Our stress may be passed on to the children in this way.


4. Are there ways that people can increase their oxytocin levels in daily life?

Dr. Uväs-Moberg: Although some are thinking about developing oxytocin drugs, I believe the absolute best thing to do is to activate your own oxytocin.  Your body knows how to handle that oxytocin.  There are several things that anyone can do:

Touch is very important.  Interactive touch with human beings is best, but it doesn’t have to be limited to human beings.  Touch happens between people and their pets.

Getting massage is helpful.

Walking, swimming in warm water, and all physical exercise is excellent.

Deep interaction, intimacy, and eye-contact are also important.

Sex releases oxytocin.

Safety is important.  For example, nursing mothers exhibit behavior associated with oxytocin when they are in a calming, familiar room.  If you move them to an unknown and more stressful environment, their safety levels fall and so do their oxytocin behaviors.  Therefore, in the latter case, their capacity to bond with their babies is reduced. In another example, studies have shown that small groups, 6 – 10 people, seem to have a positive impact on cardiovascular and cancer patience.  This may be because oxytocin is released in the safety of these settings.  Perhaps we need to make sure our family settings include levels of intimacy rather than just spending time in the same house.  Maybe our economic success, which affords us the ability to sleep in separate rooms and/or beds, has actually deprived us of the touch necessary for future success in calmness, connection, and intimacy.  When people had less money, children had to sleep together in the same beds or listen to night time stories rather than play individual computer games.  Societies at that time had built in bonding and companionship mechanisms.  We need ways to restore these to our children.


5. Oxytocin is often thought of as a female hormone.  Do men have oxytocin and, if so, how does it operate in their lives?

Dr. Uväs-Moberg: Both men and women have oxytocin and in almost the same amount.  Pregnancy, labor, and nursing activate oxytocin in women and, obviously men do not have the same activation.  But men appear to experience oxytocin when they relate to their children and they also experience oxytocin with touch.  It is both a mistake to say that oxytocin is only a female hormone and not a mistake because we do not know all the ways that oxytocin is activated in men.


6. Your research has supported the ‘Peaceful Touch’ programs in Swedish public schools. What is ‘Peaceful Touch’ and what results have been reported by the school systems?

Dr. Uväs-Moberg:  ‘Peaceful Touch’ is a program that works in a variety of ways.  One of the most important is that children are taught how to touch each other in peaceful ways.  Discipline problems have become very common in Swedish schools.  Teachers report that Peaceful Touch programs have (a) reduced the level of aggression in the classroom, (b) increased the length of time students can sit still, (c) enhanced students’ ability to listen, and (d) improved their ability to take information in.  It is important to realize that massage and/or peaceful touch is beneficial to both the giver and the receiver.   This activity is much better than giving children drugs to control their behavior.  There should be more money for good research of these programs in Swedish schools.  Oxytocin research also suggests that parents and children learning to give each other ‘Peaceful Touch’ could be very beneficial.  I recognize that ‘touch’ is a very controversial issue now, but believe that we may be able to find ways, even if it isn’t physical touch, to give our children experiences with calm and connection.


7. Are there any medical conditions that you think might be helped by oxytocin?

Dr. Uväs-Moberg:    Children like autistic children, or others who have problems opening up, could benefit from oxytocin.  But, before we start talking about medical use of oxytocin, I believe we need a new system of ethics.  Unlike other ‘feel good’ drugs, oxytocin is very subtle.  People might not even realize that they’ve taken oxytocin.  An interesting study reported in the June 2005 issue of Nature examined the role of interpersonal trust and oxytocin.  Ernst Fehr of the University of Zurich and his colleagues discovered that men who inhaled a nasal spray spiked with oxytocin gave more money to partners in a risky investment game than did the men who sniffed a spray with no active ingredient.  The researchers concluded that “oxytocin specifically affects an individual’s willingness to accept social risks arising through interpersonal interactions.”

Can you imagine this happening without people knowing they have been exposed to oxytocin?  A good thing could be used for bad purposes.  Obviously, it will be wonderful if we can help autistic children and others who cannot open to interpersonal relationships, but we need to think deeply about the ethics involved in any larger use.

8. Do you believe that there is relationship between intuition and oxytocin?

Dr. Uväs-Moberg: Yes.  Oxytocin fosters openness.  I am convinced that intuition is one branch of that opening.  For example, nursing mothers report a profound connection with their children and often intuitively know what their babies want, although the babies can’t express themselves verbally.  I believe that this knowing is an intuitive process.  There are many interesting questions about how intuition might work.  For example, what is the difference between memories and images which seem to arise from the future? How can we keep intuitive images clear and not distorted by wishful thinking or psychological reactions? These are interesting questions which should be explored someday.


9.  Assuming that you could do any further research on oxytocin that you wanted, what would interest you?

Dr. Uväs-Moberg: Two of the most interesting frontiers in oxytocin research are (1) the mental, mind, or psychological state of a person and (2) the relationship between spirituality and oxytocin.  In the former, I am interested to know if seeing images or thinking about things that relax you also causes the release of oxytocin. The neuroscientist and author, Antonio Damasio of Iowa University, raised this issue in an editorial in the same June 2005 Nature.  When asked if he thought that crowds of shoppers might be persuaded to purchase more if they were sprayed with oxytocin, Damasio referred to slick marketing campaigns that people are already exposed to.  He said that these campaigns lure, ‘you in with images of wonderful landscapes or sex, and [they] probably work in exactly the same way.” I, too, suspect that this images release oxytocin, but research needs to be done on how oxytocin works with mind or mental states.


In the case of spirituality, it may be that prayer, contemplation, and meditation also activate oxytocin, but we have no way of knowing.  Energy medicine professionals are searching for ways to measure the physiology of body energy.  To date, I do not know of any reliable way to do this, but I believe that oxytocin will play a role and that common principles may be found in the Body/Mind/Spirit interaction.

Testosterone Therapy is associated with reduction in pain in men

Leave a comment


Testosterone Replacement Therapy Doctors

Boston Testosterone Partners

Boston, Massachusetts—- New studies have associated a reduction in pain in men undergoing testosterone replacement therapy.  The results were presented at The Endocrine Society’s 95th Annual Meeting in San Francisco.

“In this study, we attempted to determine whether testosterone replacement improves pain perception and tolerance, and quality of life in men with low testosterone levels due to narcotic analgesics,” said the study’s lead author Shehzad Basaria, MD, Medical Director, Section of Men’s Health, Aging, & Metabolism at Brigham & Women’s Hospital, Harvard Medical School, in Boston, MA. “We found that testosterone administration in these men was associated with a greater reduction in several measures of pain sensitivity during laboratory pain testing compared with men who were on placebo.”

In addition to being highly addictive, opioid use is associated with a number of side effects, including suppression of the hypothalamic-pituitary-gonadal axis in both women and men, resulting in decreased testosterone production. Low testosterone, in turn, can result in sexual dysfunction, decreased muscle mass, increased fat mass and decreased quality of life.

Previous animal research has demonstrated that castration of rodents is associated with increased pain perception while testosterone replacement reduces pain perception, suggesting an analgesic effect of this sex steroid. Whether these beneficial effects can be replicated in humans, however, remained unclear.

In this study, investigators found that, compared to placebo, testosterone therapy significantly improved pain perception and tolerance during laboratory pain testing. Testosterone therapy also improved some aspects of quality of life.

“If larger studies confirm these findings, testosterone therapy in this patient population may be beneficial in improving pain perception,” Basaria said.

The study included 84 men ages 18-64 years old with opioid-induced testosterone deficiency. Their average age was 49 years. Of this group, 65 participants completed the study. Investigators randomly assigned participants to receive either testosterone gel, applied to the skin, or placebo, for 14 weeks. Thirty-six men received the testosterone gel, and 29 received a placebo.

At the beginning of the study, and then again at 14 weeks, the investigators assessed pain measures and quality-of-life parameters.

For more information on our unique Men’s Testosterone and Wellness therapies visit us at http://www.BostonTestosterone.com or http://www.Facebook.com/BostonTestosterone.

“The Greatest Health of Your Life”℠
Boston Testosterone Partners
National Testosterone Restoration for Men
Wellness & Preventative Medicine
855-617-MEDS (6337)

Older Entries