So, it’s time to settle this argument once and for all, if that is possible.  I say ‘if that is possible’ because people believe what they want to believe and there is a lot of conflicting information. So what makes me the ultimate authority on this topic?

Simple, I can back up everything I say with real research. I can back up everything I say about my product and others I have tested, with 3^rd party independent unbiased testing.  So, I hold a challenge out to anyone, who makes any of the products in question here. Test your products outside of your own company, in the same way I do.  And then, I challenge you to make it public. Somehow, I know that will not happen!

The problem in the supplement industry is that people are hiding behind marketing hype and out and out fallacies, when it comes to making statements. Sadly, the letters, PhD or MD behind the name, do not stop this problem.

I say, prove it. And I can prove what I say is true.  Can you?

So, let’s talk about how the myth of rancid fish oil got started and what it really means.

In 1974 my Dad came home with a big jug of fish oil, telling the whole family to start taking it, because new studies showed it was good for us!  Now one whiff of the stuff and you knew it was rancid.  It didn’t just smell fishy, it smelled rotten fishy.  I have no doubt it was rancid, but like a dutiful son I took it for a full 2 weeks before I finally ‘fessed up to my Dad and said “I quit!”

He laughed and told me he stopped after 2 days.

I have no doubt that fish oil from the old days was rancid.  I suspect there are some rancid brands out there still, but they must be far fewer in number. There is an organization that looks at fish oil very closely called the IFOS.  Their published recommendations for the highest grade fish oil is a product that contains less than 45 ppb PCB’s, dioxin and furan less than 1 ppt, and oxidation less than 19.5 meq/kg. The last number, the 19.5, is the oxidation value.  This is basically a measure of rancidity.

My fish oil 3^rd party independent analysis is published for all to see here.

Among any other values you might want to check, you can see we set our standards far tighter and better, at less than 5.0 meq/kg. for oxidation.

So now you know my stuff is far cleaner and less oxidized than even the toughest international standard. What do you know about other fish oils?  What do you know about krill? Nothing, except what they tell you on the endless blogs,  videos and websites.

Now let’s look at the scientific basis for the “rancidity” argument.

Fats are integral parts of cell membranes and essential to inter/intracellular signaling throughout the body. They exist as long chain “fatty acids” in the membranes and are modified and released as chemical messengers when needed,  both to the outside of the cell (eicosanoids and docosanoids) and inside the cell (resolvins).

These fatty acid chains are easily oxidized by free radical damage. This free radical damage takes place when a high energy particle known as an electron “bounces around” looking for a place to land and give up its energy.  Free radical damage to fats is particularly problematic because the energy from that loose electron can be passed from one fat chain to another in a true “chain reaction” as that electron’s excess energy bounces from one fat chain to another, doing damage all the way. Sounds bad, doesn’t it?

Well, your body has several ways to interrupt that process. Among the biggest ones are Vitamin E absorbing the free radical, a potent intracellular antioxidant known as glutathione, absorbing the free radical, or the normal and ongoing replacement of fatty acid chains in the cells. Of these 3, the role of importance is as follows: simple replacement, Vitamin E, and finally glutathione.  Please note this order only applies to fatty acids and not other things like proteins and carbohydrates where glutathione’s role is huge.

People who do not understand this say things like, “You need to take more Vitamin E if you are taking large doses of fish oil.”  This is unsubstantiated pseudo-scientific nonsense, also known as BS. It’s a classic case of someone who does not understand fatty acid biology playing smart and reading a biochemistry textbook. I wish it were that simple.  Just because a reaction exists in the body does not mean it is abnormal or damaging.

The simple fact that is left out is: You have to be Vitamin E deficient to actually not have enough Vitamin E in your body for this ever to be a problem.  Just about everyone in the Western world has way more Vitamin E than is needed to handle this problem.  I challenge anyone who makes associations with high dose Vitamin E and high dose fish oil to show me the last case history of Vitamin E deficiency they have seen in the Western world.  I also challenge them to show me a study where Vitamin E improved the clinical outcomes of any dose of fish oil. There are none.  And I can show you more studies that used fish oil alone and Vitamin E and fish oil that showed no clinical differences at all.

Zero, Zilch, Nada!

That does not mean that Vitamin E is worthless. It simply means you do not need to take “extra” Vitamin E to protect against rancid fish oil – especially if you use a high quality brand like mine that is already well below any standard for rancidity and oxidation out there. It also means that most of the reasons given for not taking high dose fish oil are the same pseudo scientific nonsense.

So where does the current round of the rancid fish oil myth come from?

According to Harry Rice, PhD, an Omega 3 researcher, it comes from a small number of animal studies using rancid VEGETABLE oil, not fish oil. These studies suggested that high doses of rancid vegetable oil (which is laden with inflammatory Omega 6 fats to begin with) might (not ‘do’) adversely affect the animals’ health.  So someone decided to equate the vegetable oil findings in animals to Omega 3 findings in humans.

Actually, there are human studies where up to 8 grams a day of rancid – yes, rancid – fish oil was consumed for 7 weeks and had no adverse effects on human health.

Now, I don’t recommend you do this experiment yourself, because I did it back in 1974 and it’s not what I would call fun.  But, the bottom line is, there is actually no proof of any damage to human health by consuming oxidized Omega 3’s. There are valid concerns about toxins in Omega 3 products as I have raised about krill and some of the “natural triglyceride” products in my lectures, but that is a different issue.

Also, remember that the oxidation of fat is a natural process.  The real way to guard against it is to take enough of your clean non-oxidized Omega 3 product to replace those fats as needed.  This is the reason I do the Omega 3 finger stick test some of you have already done. The far bigger source of oxidation in the real world is too much Omega 6 fats from vegetable sources, not rancid fish oil!

Now you don’t have to take my word for it.  You can look all this up on the internet for yourself.  Just stick with scientifically based sources of information and not Dr. so-and-so’s website! If you are wondering why some people will tell you differently, just ask this question: can they prove what they are saying other than by saying, “because I said so and you should trust me”?

That is the reason there are studies and science. Because educated guesses and opinions are just that.

Make ’em prove it! It’s your body and your health.

Doc

An 82 year old woman dies of reparatory failure – what has happened to her telomeres and what role does this play in her death?

Telomeres are non-coding, repetitive sequences at the end of the chromosome, occurring in a repetitive TTAGGG (in humans!).

When we are conceived, they are approximately 15,000 base pairs long.  Cellular replication alone is enough to shorten the telomeres because of the “end replication problem” which essentially means the DNA replicative mechanism “falls off” the end of the chromosome before they can replicate telomere segments.  The enzyme that does replicate telomere ends – telomerase – is repressed or expressed at very low levels in somatic cells. Because of the massive cellular replication it takes to go from zygote stage to newborn and the inability of most differentiated cells to express enough telomere lengthening “telomerase” to replace those passively lost pairs. Thus you are born with an average of 10,000 base pairs in your telomeres.  A telomere length of 5,000 base pairs is usually enough to induce cellular senescence ( see below).

In addition, telomeres are not linear but rather looped structures, so a “zero” length telomere is not needed to induce cellular demise.  Changing the 3D structure and interfering with the loops is likely enough to activate senescence or apoptosis. 

By newborn stage 5,000 base pairs have already been lost, leaving another 5,000 to determine the length of replicative cell life. When those 5,000 are gone and the telomere length is now reduced to 5,000 base pairs, cellular gatekeepers (like p53 and others) trigger replicative senescence.   Many “slings and arrows” of daily living can accelerate telomere loss such as stress, lack of exercise, oxidative exposures of any kind, poor diet, lack of sleep and others and increase the speed of telomere loss. Almost every disease process of aging is associated with some kind of increased telomere shortening.  The standard cell population used to measure mean telomere length is White Blood Cells for ease of acquisition and because of their relation to immunosenescence.

Studies now suggest that the fate of the individual cell is more tightly correlated to the “shortest telomere”. That means that one short telomere can induce cellular damage, senescence, or apoptosis.  The number of short telomeres many not be directly related to the mean telomere length in all individuals but the forces that shorten them are.

If cellular mechanisms fail to stop replication at 5,000 base pairs and telomere loss continues, then somewhere around 1,000 to 3,000 base pairs intracellular gate keepers should trigger apoptosis.  If this does not occur and cell division continues, the genome is unstable and this is where we feel most adult cancer occurs.

Other tissue telomere length is not absolutely the same as WBC but usually correlates well with WBC length in terms of “short or long”.  The argument has long been made that not all tissues age by telomere length.  The cardiomyocyte in particular is often cited as a way of “disproving” the telomere theory of aging.  Cardiomyocytes have longer than average telomeres.  This makes interpretation of their absolute length difficult. The theory goes since they do lose telomere length during their lifespan and do not replicate at the rate of WBC, etc.,  they “should not” be affected by telomere loss in the same fashion.  They are not. It is likely that a smaller amount of telomere shortening is required to cause mitochondrial dysfunction as Passos et. al. showed in 2010.  Telomere length, function and integrity appear to be responsible for mitochondrial mutagenesis, biogenesis and influence redox functions as well suggesting an intimate relationship between telomere length and mitochondrial health.  It is thought that cardiomyocytes accumulate myocardial dysfunction via the same mechanisms with less direct telomere loss.

A fact often overlooked by even cardiologists is that independent of whether telomere loss explains how and why cardiomyocytes age, telomere loss clearly explains vascular aging.  Cardiomyocytes (as with all other post mitotic tissue) are dependent on blood supply.  Cardiologists and cardiovascular surgeons do not restore cardiomyocytes to health, they restore the blood supply, and the blood supply clearly ages by telomere loss!

In addition it is important to know that adult stem cells – a significant part of the regeneration mechanism -also suffer telomere loss and damage, leading to the aging of this population of cells. The creation of IPS (induced pluripotent stem cells) creates embryonic like stem cells and lengthens the telomeres again, by telomerase activity.

Aging occurs when the damage to an organism exceeds the rate at which that organism can repair said damage.  Your 82 year old woman begins to lose lung tissue long before she is 82.    Repair requires the existing mass of lung cells to be able to replace damaged tissue by replication (thus inducing more rapid telomere loss)  and in concert requires a stem cell population that can supply new cells for differentiation where needed.  If the existing cell mass is in replicative senescence or apoptosis and her adult stem cell population has been damaged to the point of dysfunction, she has no way of repairing her damaged tissue.

Basically she has long since lost the ability to repair her lung or other tissues and when the reserve is gone, she dies of “respiratory failure”.

Dave Woynarowski, MD, co-author The Immortality Edge

There never seems to be a lack of people ready to volunteer their opinion on things they have no knowledge about.  A friend once told me the problem with society today is there is no shame.

I couldn’t agree more.  There is no lack of people ready to pontificate on telomeres, telomerase, and telomere biology who can barely say the words!

All kinds of moral, ethical and social machinations come out of these apparently clairvoyant people.

So it is with telomere testing.  Some of my ire is because I have addressed all this before in “Why telomeres are not the next cholesterol” and “Telomere Turf Wars, the Blasco Fiasco”.  Perhaps it’s because I did not ask for people to weigh in on the subject or perhaps not that many people read these blogs, which were highly informational.

Just this past week a slew of social networking and blog type posts claimed that short telomere testing can be used to predict the how’s, when’s and where’s of one’s mortality.

At this moment that is absolute nonsense and without scientific foundation.

Claiming that telomere testing is in a stage where it can predict the time of death or even that death is impending is just plain flat out wrong.  Spinning one’s wheels about whether the government and insurance companies will use it against us is even worse.

There is simply nowhere near enough data about who will die of what and when for any type of telomere test to be that predictive.  Yet.

That day is coming and as telomere testing becomes more common both the Mean Telomere Test (MTL) and the short telomere test that Dr Blasco pioneered will be able to help predict many of those things.

But human beings have a way of confounding even the best scientific prognostications.

After all, you can still be hit by a bus!

So once again, here is my stance.

Mean Telomere Testing is most useful in larger studies looking at population trends including heart disease, diabetes, cancer and ultimately the risk of dying.  But it is not very good for individual prognostics.

Short telomere testing is THE way to go to look at how you are personally treating your telomeres over time, especially if you are aggressively intervening on their behalf with TA-65.

But as of this moment it is still in the “gearing up” stage, meaning it is not feasible for most of us to get short telomere testing just yet.

I have contacted Dr Blasco’s company Lifelength to see what is actually involved and if they are ready.  After all, shipping blood from the US to Spain may not be very feasible and at this moment there are no labs in America that do this test.

I will continue to keep you posted in rational scientific fashion.  I am very optimistic about the utility of short telomere testing and I am certain that with the speed that the field of telomere biology is moving much of the stuff that is nonsense today will have real application sooner than later. But at this very moment all that pontification is a waste.

Like it or not, in today’s gotta-know-it-now, here-today-forgotten-tomorrow “information-” based society we’ll just have to wait a bit longer for the application of these tests.

Dr Dave

1)     While the mouse model of human aging is very useful, mice do not age by telomere shortening alone and the scientists interviewed in the article know that.  They are also aware, I am sure, of the human published trial with TA-65 showing similar results, to what has been found in mice.
 
2)     Lack of statistical significance means any finding that does not reach statistical significance is likely to be chance – and the scientists know that too. No doubt they have used that term hundreds of times with that exact meaning in their own studies.
 
3)     The oral absorption of TA-65 and/or TAT 2, is both well documented by Dr Harley and Co. and the scientists know that as well.  They have no doubt seen the same data and same slides I have that date back to prior to 2007, showing marked improvements in the immune function and reduction in various viral loads in early testing.  I guess all that happened because of the world’s biggest placebo effect and had nothing to do with the compound being absorbed orally.
 
Again, this kind of stuff is pretty much par for the course for writers who have an anti-anti-aging agenda.
 
But then they started picking on the individual scientists.
 
Thea Singer mentioned Cal Harley’s age of 58.  She did not say how old anyone else was, just Cal.  Then came the insinuation that Dr Harley was looking for a soft place to land and some financial gain from TA-65, etc.  I forgot that scientists are not supposed to make money.  They are supposed to grovel for grant money instead.  Money is bad, unless you are a journalist! My bad!
 
Still, I and thousands and probably soon millions of people, will be in debt in a non-financial way to Dr Harley for his seminal work in the field of telomerase activation and human health and longevity.
 
Also, somehow Singer forgot to mention that Dr Elizabeth Blackburn, who is one of the Nobel Laureates from 2009, is now in business with Dr Harley.  Care to comment on that Ms. Singer? Does that also make her a 50 something scientist looking for a big financial score?  I doubt it!
 
Then came the attack on poor (or maybe soon to be not so poor!) Maria Blasco, whose work on the specifics of telomerase activation and its longevity effects is second to none.
 
I wondered what got everyone so upset at Maria?  After all, she worked for and with one of the Nobel Laureates as well.
 
Then it dawned on me. 
 
She basically invented short telomere testing, which is the single most important thing for individual results and small group studies, despite the protestations against its use.  Recent articles have shown that the short telomeres are the critical ones in terms of the results of what happens to and inside a cell.

• The shortest telomere (not average telomere length) is critical for cell viability and chromosome stability. Hemann et al. Cell 107(1): 67-77

Incidentally, this paper is not new; it was published in 2001 from Carol Greider’s lab!

Ultimately the work on short telomeres means that mean telomere length (MTL), long the standard of studies on telomeres, is of marginal use when following an individual’s telomere therapeutics, especially over such a short time frame as one year.
 
It also means that we should be using that test and not the MTL for such studies, since the MTL is a pretty sloppy test.  I have read studies using a Q-PCR MTL analysis, claiming a near miraculous telomere lengthening after 90 days.  Given that the Q-PCR varies by a standard deviation of 1,000 base pairs, I find those results questionable.  Same with the FLO-FISH, which while twice as good, still has a huge variability gap.
 
Clearly MTL is very useful but only in the right situations. It only takes one short telomere to send a cell into senescence, crisis or worse.

In vivo telomerase finds the short telomeres first and fixes them first and in many cases exclusively.  That is the natural order of things.  It may be speculation, but it seems that any meaningful improvements in MTL come from the lengthening of short telomeres in the first place.
 
More outrageous was the insinuation that Maria Blasco’s TA-65 study deliberately coincided with the launch of her new company, Life Length, which is devoted to measuring short telomeres.  Anyone with even a tiny bit of business sense knows that starting a biotech company requires investors and venture capitalists.  I highly doubt Dr. Blasco was able to conveniently arrange for her investments to coincide with the exact date of the TA-65 study.  I highly doubt that was even a consideration.  Still, I am glad it happened.
 
Then again, I am just a dumb doctor – not a brilliant researcher.  But I can see why people are upset with Maria Blasco for changing the rules of the game and ushering in a really meaningful way for those of us who individually want to follow what is happening to our telomeres.
 
For the record, I think all of the scientists involved in the “Blasco Fiasco” are brilliant.  But of course Dr. Harley and Dr. Blasco were not asked to comment.  Neither was another brilliant scientist, Dr Bill Andrews, who discovered the human telomerase gene.
 
I found Ms. Singer’s article pretty repugnant on many levels, but not surprising I guess.  It made me wish scientists would concentrate on being scientists.  It made me wish all of the scientists in this field would get the professional courtesy, recognition and yes, money they deserve for ushering what must surely become the biggest discovering in the history of human health and longevity.
 
Finally, I wondered why Thea Singer would take such a stance, other than what has already been mentioned.
 
Maybe her book is not selling.
 
Ours is doing great.
 
Dave Woynarowski, MD – co-author The Immortality Edge

These people are very smart and well meaning.  But in their attempts to educate the public as to the very real importance of telomere length and its predictive value for overall health, I think they have inadvertently created a misconception.

The standard measurement of telomere length is called WBC MTL. It stands for white blood cell mean telomere length. The two ways of doing this test are called QPCR and FLO-FISH. The QPCR has an agreed inaccuracy of about 1000 base pairs of telomere DNA. This translates into about 5 to 10 years of aging or aging reversal just as a function of the test. In other words there is a pretty big error.  The FLO-FISH is a bit better with an inaccuracy of about 500 base pairs.  One way to get a more meaningful value is to wait longer to do the test.  Like 2 or 3 years!  Often studies show tests done in a few weeks or a few months after the initial intervention was begun.  They pronounce gigantic leaps in longevity in 6 weeks for things like green tea.

This is simply not possible and is a function of the inaccuracies of the test.  In other words it’s absolutely meaningless! Yet there are some pretty big names in the field still using this test to make positive pronouncements.

One of the most appealing things about TA-65 is that a group of people were tested using what is, in my opinion, the only meaningful test there is for telomere length: short telomere testing.

Studies have shown that the shortest telomere is the one that does the damage and therefore the most important- maybe the only important one in the bunch so to speak.

This is yet another reason why TA-65 is really the only thing that has been proven to work for addressing telomere length. It transcends the errors in testing and works exactly where it needs to to combat aging!

Sadly, until short telomere testing becomes a widely available test, which it is not (only one lab does it in Spain!), testing telomere length the current way will mean waiting 2 or 3 years before seeing meaningful results in the typical MTL tests.

Doc

So whenever I see a “typical traditional medical stance” I always feel compelled to call them on it when it comes from Mother Nature, not big Pharma. You see, they still send me all those free journals and magazines that “real” doctors read.

One of these rags published back to back articles on psoriasis, a skin condition that leads to unsightly scaly skin plaques and has other consequences including arthritis and in some cases heart disease.

The first article was about drugs that reduce “TNF” also known as tumor necrosis factor alpha, a commonly used lab marker for inflammation.  Big Pharma has scored big with TNF inhibitors for psoriasis and autoimmune disorders.  They were excited to report a nearly 50% drop in the heart attack rate in one of their studies using these agents.  They neglected to mention that Mother Nature has her own anti-psoriatic TNF inhibitor know as fish oil, which reduces heart attack rates dramatically without the side effects of outrageous costs of these fancy and sometimes dangerous drugs.

Go figure.

The next article went on to lament serious heart disease acceleration by another class of anti-psoriasis drugs known as “biologic monoclonal antibody therapies”. Their names are nearly unpronounceable and end in “mab”.  These new wave star players showcasing the Pharmaceutical Industry’s technologic prowess and advanced thinking. They are astronomically expensive but of course insurance pays for them (uh, who pays for insurance?!)  Only trouble is they cause heart attacks.

OOPS!

To Big Pharma, at this point I say, “Do nothing, you’ll be just as productive.”  And take your fish oil!

Doc

Since the realization of telomeres’ importance, there’s been an explosion in regenerative and longevity medicine.  Scientists are starting to uncover and do the unthinkable.  They’re uncovering new ways to extend life, and most importantly improve the quality of the lives they’re extending.   Instead of a feeble, sick, blind and deaf 100 years, you and I can expect a sharp, vibrant and enjoyable 100 years and beyond.  It’s a long and healthy life, very different than the inevitable decline our parents and grandparents have or are experiencing.

And we have the junk at the end of our DNA to thank.

Every day it seems new research supports and reaffirms that cancer is a disease of short telomeres, heart disease is a disease of short telomeres, Alzheimer’s is a disease of short telomeres, among many other disease “symptoms” of aging.  (I call most of the ailments we call diseases “symptoms”, because the real disease is aging and all of the other so-called diseases are merely symptoms).

In the past few months telomere shortening has shown up to 400% relative risk in cancer versus long telomeres.   The group with short telomeres had deadly, nasty and rapid cancers with little hope of survival.

Shortened telomeres create inflammation through a unique pathway very different than the inflammation that is caused by poor diet, lack of sleep and a sedentary lifestyle.   The inflammation caused by telomere erosion plays a vital role in all diseases of aging. 

Antioxidant has been a buzz word in the health industry for several years now, but telomere erosion requires extremely potent anti-inflammatories to combat the accelerated damage our bodies experience as more and more of our cells’ telomeres reach critically short levels.  These super antioxidants help slow telomere loss and are discussed at length in The Immortality Edge.  They include omega-3 fish oil and CoQ10 which have both been shown to reduce rapid telomere segment loss in cells. 

You already take fish oil?  Probably not enough.  CoQ10 is part of your supplement regime?  Are you sure you’re taking the proper form?  Read The Immortality Edge supplement plan and you’ll never have to guess whether you’re taking the correct dosage or right form of a nutrient and making the proper lifestyle choices to truly extend your lifespan and healthspan.  You’ll know.

Don’t treat your telomeres like junk.  If you want to live to see a healthy active 100+ years, read the book, implement the plan and I’ll see you in 100 years.

Afraid it’s too late?  Worried that your telomeres are shot, too short to even bother preserving?  Well, after years of screening over 250,000 compounds a natural supplement was found, tested and proven to not only stop telomere shortening but help lengthen telomeres as well.  It’s called TA-65, and it’s also covered at length in The Immortality Edge.  Everything you need to know about how to extend your healthy years is laid out in one comprehensive and easy-to-understand book.

It’s never too late to treat your telomeres like the treasure they truly are!

During my years of medical practice I was approached by patients with real fears that they were doomed to repeat their parents’ deaths.

We learned this fear was unfounded and unnecessary when we sequenced the entire human genome several years ago.  We now realize that 70-80% of whether we become afflicted with illness or disease is within our control.  The lifestyle modifications recommended in The Immortally Edge are crucial to help prevent the ailments we once believed resulted from the cruel and inevitable roll of the genetic dice.

Your genes act like a library containing many books.  Your epigenome represents the books you check out and actually read.  This is how you “change your fate”.

One example of this is related to how our body converts plant Omega-3 and Omega-6 to a useful and necessary substance called Prostaglandins that our cells need to function properly.  Prostaglandins are formed by the metabolic conversion of EFAs (essential fatty acids).  The conversion requires enzymes which assist with the conversion over several steps.  Once EFAs are converted to Prostaglandins, they work similar to hormones to help cells maintain normal functioning.  Prostaglandins appear to be involved in nearly every body function.  Various Omega-3 and Omega-6 Fatty Acids form different Prostaglandins with different activities.  A proper balance of Omega-3 and Omega-6 is important for maintaining health because they compete for the same enzymes for conversion.  Only 5-10% of Linoleic Acid (found in all oils) and Alpha-Linolenic Acid (found in flax, hemp, chia and black currant) converts to our body’s much needed Prostaglandins.  Some people lack the conversion enzymes and don’t convert any of the plant based Omega-3s.

You may be genetically predisposed to Prostaglandin deficiencies because you lack the enzymes to properly convert Omega-3 and Omega-6 intake.  You wouldn’t know you were among the misfortunate genetic group, but luckily you have the power to override this genetic misfortune by taking an Omega-3 fish oil supplement. 

Inadequate Omega-3 EPA and DHA intake can lead to low IQ, allergies, heart disease, breast and prostate cancers.  You can wait for reliable genetic tests to identify these various and sundry gene problems, or you can act now and avoid the risks involved with low Omega intake and conversion.

I recommend 6 grams of fish oil a day to help you avoid becoming a genetic time bomb!

Best in health,

Dr. Dave Woynarowski, MD, CPT

As a matter of fact, if you have read any of my emails, you know how effective fish oil is for so many things because it is a building block, a hormone, and immune modulator and anti-fat compound and more.
 
But let’s stay focused on the brain.  Fish oil’s effects on the mood and its improvement in depression were thought to be solely due to improved levels of serotonin, a natural brain chemical that blocks depression.
 
But recently it was discovered that fish oil works via the endocannabinoid system as well to elevate mood and relieve anxiety among other symptoms.
 
How does it work?  Here is a quote: “It corrects the deficit in the signaling of the CB1 cannabinoid receptor in the prefrontal cortex of the brain. This protein — the CB1 cannabinoid receptor — has been linked, over the last decade and in various studies, to depressive disorders.”
 
Well you did ask!
 
Actually restoring the balance to brain signals is just one way fish oil works; it also is an important building block that can affect memory, intelligence, hand eye coordination and many other brain functions.
 
For now, suffice it to say, you should be taking it every day!
 
I recommend a minimum of 3 grams and prefer most people to be on 6 grams. That should keep you naturally high!
 
Best,
Doc