Monthly Archives: July 2011

Blueberries: Super Food and Fat Cells

Blueberries:  Super Food and Fat Cells

Competency:  Really Good Food

Reference:  Science Daily, April 11, 2011 from a presentation at the Experimental Biology 2011 meeting for the American Society for Nutrition on April 10.

Michigan blueberries are in!  And I can’t help but note this research news that came across the wires a month or so ago.   Blueberries help fight the development of fat tissue!

Shiwani Moghe, from Texas Christian University, decided to test whether fat cells growing in tissue culture would have a reduction in their differentiation by blueberries.   What she found was that they did.  And a lot.  She found that the more blueberry polyphenols she put in with the fat stem cells, the more the tissue culture stem cells refused to change into mature fat cells.  The blueberry polyphenols reduced the differentiation into fat cells by up to 76%.  “I wanted to see if using blueberry polyphenols could inhibit obesity at a molecular stage,” said Moghe.

This is very, very basic science on stem cells from mice, so in no way can be shown to be proof for humans.  But I suspect she won’t have any trouble finding volunteers to give away a few human fat cells for research.  I have a few right here to share.  It’s the picture that’s being painted for polyphenols from all plants that matters.  This column has reported how Dr Joseph from Tufts found that rats with Alzheimer’s, when fed 10% of their calories as blueberries, never developed Alzheimer’s.  There have been other reports that blueberries, eaten regularly, reduce the risk for developing metabolic syndrome.  Metabolic syndrome is what we all have when our blood sugar is a tiny bit high, our blood pressure a tiny bit high, our cholesterol a tiny bit high, but we aren’t sick yet with anything.  Reversing metabolic syndrome is part and parcel of preventing Alzheimer’s.  Ditto for heart disease.  You can see the implications of this spreading.

The Tufts research group developed a concept called the ORAC score, which stands for the potency of the anti-oxidant ability of different foods.  ORAC stands for Oxygen Radical Absorption Capacity.  Blueberries get about a 3500 for a serving (1/2 cup).  Bananas get 100.  Many berries get scores over 2500.  And in general, the brighter the color, the higher the score.  Goji berries and Acai berries are even better, just way more expensive.  Pomegranate is another particularly good score.  We should all try and have about 10,000 ORAC points a day.  Blueberries are best!

And it may not be the anti-oxidant quality that matters.  It may be that these polyphenols talk directly to the inflammation source and turn off NKκB, our “uber-controller” of inflammation.   Even better.  Blueberries appear to be stars!

WWW. What will work for me.  I just went to Brennan’s and bought fresh Michigan Fat Boy Blueberries.  Picked at the peak of the season, they are the highest ORAC score of them all.  And I eat them every day on my cereal year around.  Try some!

A Cure for Alcoholism

The Cure for Alcoholism by Roy Eskapa – A Book Review

Competency:  Addiction Control

Date:  July 20, 2011

Cure for Alcoholism!  My goodness.  Either this is a pure hoax or a huge advance, but it most certainly is controversial.  Where on earth does this idea come from?  From what I know only 15% of alcoholics ever get help with some sort of 12 step program, and then only 15% ever succeed.  This book talks about a method that to date has resulted in a 78% cure rate for alcoholics.

I bring this book forward because last week we talked about the melanocortin system in our brains and pituitaries.  In brief review, the melanocortin system is the integrative hormonal symphony that blends our energy, our cortisol, our pleasure and our stress responses.  One of it’s products is beta-endorphin, our natural opioid.  And if you take naltrexone, a blocker of opioids, you can get folks to lose weight with a long term approach.  That’s nifty.

Well then, this is the same story with a different addiction.   Alcohol is particularly wicked in its destructive capabilities so I’m full of skepticism when I read this book. But now I’m a cautious believer.  I’ve been convinced.

This is how it works.  It’s called the Sinclair method.  The method is simple.  Take low dose naltrexone every day and keep drinking.   No judgment.  No punishment.  Don’t change behavior.  Just keep on with your normal addictive drinking.  The naltrexone makes a normal person feel, well, nothing.  A non addictive person wouldn’t know they had taken a pill.  An alcoholic also doesn’t notice anything either.  But underneath the surface, their brain is being rewired.  It does not work in 20 minutes, or even 3 weeks.  It takes three to four months for the wiring in your brain that is caused by endorphin reinforcement and released by alcohol to become deprogrammed.  An alcoholic has neural pathways that make him/her think about alcohol, crave it and want to drink it.  Those pathways become progressively stronger and more reinforced every time they are bathed in another dose of beta-endorphin that is released by wine, or beer, or gin ingestion.   The naltrexone deprograms that.  It blocks the opiate reinforcement.   You don’t want to encourage huge quantities of alcohol.  But every small session is another deprogramming session, so frequent episodes of lower response helps deprogram the addicted, hardwired, compulsive alcoholic brain.  In fact, maybe any addictive behavior…?

You don’t even have to be an alcoholic to benefit from it.  If you know that you tend to drink a bit more than you want to on occasion, and would like to cut down, you can get yourself in a much better spot by taking the drug before your parties, and you will find yourself gradually being in more control, wanting less alcohol, and drinking less.  (You still can’t drive.)

WWW. What will work for me?  Get where I’m going.  How much of your eating is addictive?  Want to lose weight?  Read this book.  See what you think.  There may be more truth in this for many addictive situations.  Which one is yours?  There may be a means by which you can get help.  One more impact of the melanocortin system.  That’s why it’s important to learn about this stuff.

 

Written by John E Whitcomb, MD

Brookfield Longevity and Healthy Living Clinic

19585 W North Ave, # 160

Brookfield WI 53045

www.LiveLongMD.com

262-784-5300

Melanocortin System and Obesity

Melanocortin System and Obesity

Reference:  Biochem J  2010 May 27;428(3):305-24  and Eur J Pharmacol Jun 2011 June 11;660(1)1;181-7

Competency:  Weight Loss and Weight Control

You can’t just dive in and lose weight?  Having trouble with being a little overweight?  It seems so simple.  Eat less and exercise more!   Well, not so easy.  Which is why we are all getting fatter.  Have you ever heard of the melanocortin system?  I hadn’t.

One tiny column is hardly enough to teach you much, but it’s an idea you need to know about, even if just in name.  Let me give this a try.  Your brain makes a large protein called pro-opiomelanocortin or POMC for short.  It can be broken down into 7 different shorter pieces, all called collectively the Melanocortins, hence the melanocortin system.  One is called endorphin (your natural opioid).  That deals with pleasure and pain.  Another is melanocortin with stimulates melanocytes.   That is all about skin and hair color.  But it is  also complex because they can stimulate appetite, blood pressure, inflammation, skin and hair pigmentation and bone growth.  Whew.  And then there is ACTH, another of the 7 peptides that come from POMC.  It stimulates the production of cortisol.

Finally, there is lipotropin that is all about fat.  And here is where we spin off into leptin and its feedback loops with serotonin and first and second order neurons giving varying levels of feedback.  Confused yet?

The reason this matters is that we are beginning to understand and make the connections between why women gain weight around menopause and just can’t lose it for the life of them.  It sticks like glue.  Unless you mess around with the opioid suppressor system.  And if you have polycystic ovarian syndrome, this is all about you.

What’s that?  Naltrexone is an opioid blocker and low dose naltrexone is one of the first coarse methodologies discovered that works with blocking the dysfunctional aspects of the melanocortin system.  Haven’t you ever felt like eating was an addiction and you just couldn’t stop?  Can you imagine what your brain is saying when you are 8 scoops into the icecream bucket?  (YES!!!)  What we find in the second paper is what happens when women start losing their estradiol with menopause.  In the brain, estradiol is used to enhance the expression of POMC.  As it drops out of the picture, fat mass increases as a way to make more estradiol via the enzyme aromatase that happens to be in fat tissue.  You gain weight to make more estradiol.  And that makes your brain happy.  Wouldn’t it be easier to just give you a wee bit of estradiol….just a smidgen?

Now, interestingly enough, if you want to lose weight, you can take low dose naltrexone and bupropion and you don’t level out because you have blocked the endorphin negative feedback effect.

WWW. What will work for me?  This is one of those way-over-the-top ideas I’m trying to get my head around.  But it may be the beginning of a larger conversation.  The road to successful weight loss may be around this corner.  Certainly we are seeing that low dose naltrexone works with weight loss in some overweight folks, particularly if they have Polycystic ovarian syndrome.  As for me, I’m just a hunkering down and trying to focus on having an apple instead of ice cream for my bedtime snack.  My endorphins would be happier if I had the ice cream.

Written by John E Whitcomb

Brookfield Longevity and Healthy Living Clinic

17585 W North Ave, Suite 160

www.LiveLongMD.com

262-784-5300

Vitamin D and Diabetes, A Randomized Placebo Controlled Trial Shows the IOM was too Cautious

Vitamin D and Diabetes, A Randomized Placebo Controlled Trial Shows the IOM was too Cautious

Reference:  AJCN July 2011 Author Joanna Mitri from Harvard School of Public Health

Competency:  Vitamin D

Yeah!  A Randomized placebo controlled trial that unequivocally shows that Vitamin D works with diabetes in improving pancreatic function.  Dr Mitri and her team had to work hard to get this study done. They had to screen over 911 subjects to get 44 perfectly matched folks with diabetes that were split into 22 and 22 subjects.  They had 45 in a parallel control group who got a bit of calcium as their treatment option.  The study only ran for 12 weeks but that was enough to show meaningful changes. What did they look at?  The ability of the pancreas to secrete insulin and control blood sugar is the whole story of diabetes.   This study looked at a composite index of pancreatic function and showed that the Vitamin D group improved their function by a score of 300 while the control group dropped 126 points.  That was statistically significant to a very high degree.

As we get heavier and put on weight (these folks were average BMI of 31) we soak up more vitamin D into our fat tissues.  It’s hard to raise your D level when you are overweight.   In this study they only raised their Vitamin D levels from 24 to 30 ng with the 2000 IU dose they gave.  So, that was cautious to say the least.   But the study only ran 12 weeks.   Readers of this column will know that 2000 IU will raise your blood level about 20 ng if you stick with it for a year.   And from our Antarctic study, we know that 2000 IU will never get you much higher than 30 ng, which is about what this study accomplished with folks living in Boston where they had sunshine, some of the time.

What’s the meaning of this study?  It’s huge.  We ALL have diabetes risk as we get a little chubby.  Much of it is subclinical.  If you have a blood sugar of just 102, your doctor will tell you to lose a bit of weight and exercise more.  Now, the script changes.  Lose weight, exercise more and make sure you are on at least 2000 IU.  We know from the American College of Cardiology meetings last year that Vitamin D levels of 45 and above correlate with reduction in cardiac risk of some 70%, so a level of 30 is cautious, but in the right direction.

This is the first good RCT (randomized placebo controlled trial) of 2000 IU on diabetes that I’ve seen.  This is good science. We now can unequivocally state that any recommendation of Vit D less than 2000 IU for someone at risk for diabetes is not enough.

WWW.  What will work for me.  Well, I want a D level of 60-80 by my read of the literature.  But I’m projecting from physiology studies that show continuing improvement in function.  This is a study showing outcome to match.  We now need the same study giving 5000 iu a day, and just aiming for blood levels of 60. ng  It’ll come.  And I’ll try not to gloat.  (And my two minutes are now up.)