Monthly Archives: September 2014

Quercetin – A Novel Super-Antioxidant

Quercetin for Cancer, Bones and Allergies

References:  Tsuji J Bone and Min Metab 2013, Mei JCAM 2013Kaur JNCI

What’s Quercetin?  You probably haven’t heard of it.  It if a flavone antioxidant that is present in lots of vegetables.  Onions and apples are always cited and there have been off and on news articles about quercetin helping reduce prostate cancer and breast cancer.  But Quercetin is in lots of other foods that you may not eat as often like capers, cilantro, kale, watercress, cranberries and plums.  In fact, many of the cancer reducing effects of vegetables may be attributable to the beneficial effects of quercetin.

So, just how does that work?  There appear to be a variety of pathways in which quercetin inhibits cancer cells.  Slowing down the rapid cell cycle of cancer cells and inducing them to die when they are meant to (apoptosis) be one of quercitin’s strong points.  It also binds to the estrogen receptors found in breast cancer and also in other solid tumors.   One study showed that it binds just as tightly as tamoxifen.  Because of that effect, it slows the multiplication and spreading of breast cancer cells.   When you combine quercetin and curcumin (sounds like a recipe for curry) there is evidence that you can slow the development of polyps in family’s that make multiple colonic polyps.  So, it slows the cell cycle in cancer and seems to increase the rate at which cancer cells initiate their auto-destruct cycle, something normal cells do on schedule.  That should make quercetin a must for all cancer patients.

What does it do for bone health?   Just about every woman in America should be concerned about keeping her bones healthy, and just about every woman is slightly on the low side.   We have a whole class of drugs that inhibit the natural resorption of bone (alendronate and friends) that have not lived up to promises – too many horrible side effects.   This is where quercetin shines.  It promotes the stimulation of new bone.   Taking drugs like prednisone (sometimes necessary for some illnesses) really thins out bone.   Compared to alendronate, quercetin is better at preventing that.   Just 150 mg a day and you can protect your bones!

There are other effects of quercetin that make it a valuable supplement.   It has been shown to tune up mitochondria.   Does that means better sports performance?  In one study of young swimmers, there was no measured effect.  But another study showed a clear beneficial effect based on measuring oxygen consumption.   And it’s mentioned in many sources for helping congestive heart failure.   It is also a great allergy medication and has been shown to reduce allergic rhinitis in folks with seasonal allergies.

What’s happened to the quercetin content of our foods?  As farmers develop foods to taste sweeter, look prettier, produce bigger yields; they have also reduced the quercetin content.   “Wilder” more original plants have higher levels of all anti-oxidants in them compared to the modern version.  For example, crab apples have more antioxidants and quercetin than modern grocery store apples.

WWW.   What will work for me?   I’m fascinated about the concept of our wilder foods having more cancer reducing effects in them compared to our modern, sweeter and prettier looking versions.   Our modern diet has less quercetin in it because of the genetic engineering of our foods, and our penchant for sugar and packaged convenient foods.   Quercetin may be one of those “pivot – point” foods that provide a bunch of benefits that are loosely ascribed to eating more vegetables.  I’ve tried it now for sneezing and I think I sneezed less this weekend.   I took 500 mg two days in a row.  But ragweed is almost over.  But I’m going to be talking about quercetin to my cancer clients.  Beat me to the punch and get on 500 mg a day.

(Want to read a great review article with lots of References: Check out Life Extension Magazine, Oct 2114)

Pop Quiz

  1. Quercetin is an antioxidant found in most meats and cheeses.  T or F

False.  In many fruits and vegetables (none in meat), but not all.  Apples and onions get mentioned a lot.  Cilantro and capers are superstars.

  1. Cancer cells don’t multiply as fast when exposed to quercetin.  T or F


  1. Cancer cells get prompted to die on time instead of hanging around when exposed to quercetin.  T or F

Right again.

  1. Quercetin might be as good as many modern bone density drugs for those with osteopenia.  T or F

True, particularly if you have to take oral steroids.

  1. Quercetin may be a great allergy pill substitute.  T or F


Artificial Sweeteners Make your Fatter

Artificial Sweeteners Make your Fatter

Reference:  Nature Sept 2014 Nature Suez

All right, you are a little overweight and want to slim down a touch.  Instead of fully sugared soda, you decide to get just the zero calorie soda instead, sweetened with an artificial sweetener.  You won’t gain weight, right?  In fact, you can drink that all day long and not put on any pounds because you aren’t eating any calories. Right?


Increasingly we are aware that our behavior is driven by forces other than our conscious, advanced brain.  In fact, it’s pretty well established that it’s hormones that drive our eating behavior.   We used to say you got fat because you were a lazy slob and didn’t exercise enough, ergo – your personality is flawed and it’s your fault that you are fat.  If that were true, you would lose weight when you ate less and exercised more.  Well, that approach has failed.  We now know that to lose weight you have to manage your hormones, most notably your insulin, which requires you changing the foods that make your secrete insulin.  Insulin and leptin are the hormones that drive your eating, and your weight gain.

So what does this study show?   Very interesting.  This happened in mice, not humans (yet) but it raises a new principle that is an open door for further inquiry.  Mice, fed water sweetened with sugar versus artificial sweetener were followed for a variety of metabolic effects.  What Dr Suez found was startling.  The artificial sweetener mice became glucose resistant, the first step to diabetes.   The source of that resistance was in their gut bacteria, not in their own chemical structure.  That wasn’t all the scientists did.  With that finding, they found that they could prevent the effect by killing off the colonic bacteria by treating with antibiotics.  Further, they could transfer the glucose resistance to germ free mice by doing a fecal transplant and giving the germ free mice the colonic bacteria that caused the glucose resistance in the first place.    Finally, they identified the metabolic pathways that were altered in the bacteria that altered their host’s glucose tolerance, and found that those same pathways exist in humans.

Did you get that core idea?  An alteration of gut bacteria caused glucose intolerance and insulin resistance.  That’s diabetes, or the first step.  The sequence is then as follows.  When you are glucose intolerant, your insulin level rises.  Insulin causes your fat cells to take up calories and your liver to make more fat.  Those calories aren’t available for activity so the body feels hungry and eats more food.  You gain weight.   And the net effect was all started by changes in colonic bacteria, brought about by the artificial sweetener.

One more time, we have to run the sequence of events that leads to obesity.  It’s exactly opposite to what the American Diabetes Association teaches when it says it’s your fault for eating too much.  The too-much-food-theory is NOT primary cause, it’s a secondary effect. What is primary is eating the wrong food that causes hormonal responses.  In this case, the hormonal response is actually metabolic changes in your gut bacteria.   Your colon is not just a waste dump, but a vibrant, active organ that controls much of your metabolism.

The cool thing is that you can change your behavior. Stop using artificial sweeteners.  Just stop.  Stop.  Quit.  Drink Water.

WWW.  What will work for me.  Water.  Tea.  Sour flavors.  Just no artificial sweeteners.   (Stevia was not measured, and being based on a plant is an unknown quantity.  I’m still using Stevia. Trying to make it less.)


Pop Quiz

  1. Mice that eat water sweetened with artificial sweeteners have no metabolic effect.  T or F

Go to top of page and re-read this article.  They became glucose intolerant

  1. When you are glucose intolerant, you gain weight.  T or F

True.  May be chicken or egg, but with high insulin, you more easily push calories into storage.

  1. The primary cause of the glucose resistance in these experimental mice was in their gut bacteria.  T or F


  1. The glucose resistance could be transferred to other mice that had been grown in a perfectly germ free environment, simply by giving them a fecal germ transplant.  T or F


  1. The same pathways that cause this glucose intolerance are present in humans, but not tested yet in humans.  T or F


Leptin: A Primer for Weight Control

Leptin: A Primer for Weight Control

Reference: Annals of the New York Academy of Sciences

Just what is leptin?   Nice that you would ask. You have likely heard about it and remain slightly fuzzy. Isn’t it “one of those obesity hormones?” you might ask. Well, yes. It is the hormone made by your fat cells that circulates back to your brain and tells you to stop eating. The bigger your fat mass gets, the more leptin you have circulating in your blood. Your hypothalamus has leptin receptors in it that read the level of leptin and set off a cascade of effects as a result. The net effect is that you turn off appetite and increase activity. All that is well established in mice and rats with proven pathways. Is it the same in humans?

In humans the connection isn’t quite so sure. There is more inter-person variability than can be explained by fat mass variability, so it’s not quite so tightly linked. And gender is a dramatically different marker in humans. Women have much more leptin than men for any given amount of “fat mass”. Teleologically, we needed women to have sufficient calories in storage (fat mass) to be able to survive a winter while being pregnant. That would mean we would have had natural selection pressure to favor a balance of calories that maintained a certain fat quantity in a woman’s body. Leptin is not a satiety factor in humans because changes in food intake do not spark a short-term increase in plasma leptin levels. It’s the total fat mass that matters.

The story of leptin may boil down to orexigenic and anorexigenic stimulation. Orixigenic is what you feel when you drive past Kopp’s Icecream. Just being there, your appetite goes up. Leptin down-regulates orexigens. Turns them off. Appetite plunges. Things called NPY (neuropeptide Y), MCH (melanin-concentrating hormone), orexins, and AGRP (agouti-related peptide).   We humans are pretty complicated. Leptin also turns on or up-regulates your appetite supressors with stimulation of things called alpha-MSH (alpha-melanocyte-stimulating hormone), which acts on MC4R (melanocortin-4 receptor); CART (cocaine and amphetamine-regulated transcript); and CRH (corticotropin-releasing-hormone). Again, appetite plunges. (Remember all these words for the next time you play Scrabble)

With all that fire power, how come leptin doesn’t work to down-regulate obesity? That’s the big question. Overweight humans have very high leptin but become leptin resistant. If you give leptin to overweight folks, they don’t lose weight. And during starvation periods, the fall of leptin levels happens faster than the fall in fat stores. The conclusion is that the leptin system evolved primarily to protect us when we were starving, but doesn’t know what to do with us when we get overweight. Most of human history has had a 6 month period of calorie challenge (dry season in Africa, cold in Asia) during which we had to have a supple system of energy conservation. Now, in energy abundant times, we don’t have the natural endocrine system inside us to resist food signals. Our feedback system just doesn’t work at the top end of calorie excess.

WWW. What will work for me. Leptin had some promise a few years ago. It’s talked about a lot but hasn’t quite produced the results we want. I suspect there will be some connection to the wicked effects of sugar somewhere, but that remains a suspicion, not a proven fact. For now, we are left painting the bigger picture, and trying to understand the continuing puzzle. It’s a topic you should just know on general principles.


Pop Quiz

  1. Leptin is the hormone that fat cells put out to tell the brain that there is enough energy being stored? T or F


  1. Leptin levels rise with obesity, T or F


  1. Orexigens are internal hormones that stimulate appetite. T or F


  1. Leptin is turned off with starvation and weight loss, allowing appetite to soar and food intake to increase. T or F

That’s it. You have felt all that.

  1. The administration of leptin to overweight folks hasn’t resulted in weight loss. T or F

Again, true.

High Fat Diet WINS!

Reference:  Annals of Internal MedicineNew York Times

The first ever, randomized diet that does not restrict calories (which no one can do) and simply compares a low fat diet to a high fat diet is now published and in the books.   The low fat folks were told to cut fat to below 30 % of calories and eat more fruit and vegetables and whole grains.   The participants were racially diverse and ended up with 60 in the low fat group and 59 in the low carbohydrate group.  Those are good numbers to create statistical significance.   At the end of the study, the low carb folks had lost 8 pounds more than the low fat group.   More importantly, the low carb group lost body fat and increased lean muscle mass.  The low fat group did the opposite, losing muscle and gaining fat.  The high fat group was encouraged to eat more meat, mostly chicken and fish, but butter and red meat was allowed.  An analysis of their food intake showed that they got to about 13% of their calories from saturated fat,  more than double what our “health leadership” advises. (<6%).

But, wait, it gets even better!  The low carb folks saw their blood markers of inflammation and their triglycerides plunge.  Their HDL’s (good cholesterol) rose.   Blood pressure, total cholesterol and LDLs didn’t change significantly between the two groups.   But the low carb group did so well overall that their actually lowered their cardiac risk scores according to the Framingham Criteria.

My interpretation of this data is very simple.   Here is the context I believe it fits in.   Carbohydrates are foods that become available to eat only at the end of the growing season (fall).  The fall precedes winter, the starvation season.  Throughout human history, we have had to adapt to long stretches of lean food times, during which we had to eat meat or die.  Our metabolism had to learn to adjust to diets high in fat and protein.  Carbohydrates, on the other hand were always short term affairs.  When they became available, we would eat whatever we could get our hands on (quickly before someone else ate them, or their rotted, or frost came).   When you eat lots of carbs, your blood sugar rises, your insulin rises turning on fat production,you’re your blood fats rise.   All in tandem.  Our blood fats simply represent the transport of fat from our liver, where they are made, to our fat stores, like our bellies, hips, thighs, underarms….  Our LDLs are essentially semi trucks, the bodies 18 wheelers, if you will, moving our fats along our bodies interstate arteries to their destination.  When you stop eating carbs, you stop producing LDL fats and triglycerides.  You reduce the need to transport those calories to their destination warehouses, fat cells.

That interpretation is exactly opposite what our current health system teaches.  It says you get fat because you eat fat.   That is now disproved by this study.   We need to recognize that our body makes it’s own fat for its own purposes.  Eating carbs turns on endocrine responses that then drive how our body handles those calories.   Same effect with fats.  When you eat fat, you feel full.  And effortlessly and smoothly, your body gets the message, “It’s fat eating season, must be winter.  Time for our fat cells to open up and share so that we can make it through the winter”.

WWW. What will work for me.  I just had three eggs and a sausage made in butter for breakfast.  I won’t be hungry till lunch time.  It was yummy.  And my Framinghan score just got better by doing that.  Lunch…..hmm, a burger with no bun? And no fries!

Pop Quiz

  1. Eating a high fat diet will make you fat.  T or F

This is a trick question.  If you eat high fat and high carb, you will get fat because of your response to the carbs and subsequent turning on of insulin, which will make you store both the fat and the carbs.  But if you lower your carbs, and eat fat, you feel full.

  1. If you want to lose weight, you will lose more with a low fat diet.  T or F

False. Go back and read this study. Backwards.  You lose weight much better with low carb

  1. Eating a high fat diet can lower your Framingham risk scores.  T or F


  1. Your HDLs (good fats) will improve better if you eat less red meat.  T or F

False, false, false.  It’s backwards again

  1. You have to count calories to lose weight.  T or F

False.  You eat till full with a low carb diet, and you will lose fat weight.

Sleep Apnea – A Cure?

Reference: Science Daily, Sleep Medicine 2014

Sleep apnea is increasingly being recognized as a huge risk for men. It keeps climbing up the risk ladder as causes of heart disease.   What is it? It’s the subtle collapse of the upper airway that blocks normal, effortless breathing while asleep. What ensues is a tug-of-war between effort to break that blockage by increasingly rigorous efforts at breathing, and need for deep, restful sleep. In its most classical form, the person breaks through their apnea with a sudden snort or loud snore after a variable period of silence. Observing the sleeping person in that silent period will show someone who almost looks like they are gagging, as they make an effort to breath in, but have it arrested by being unable to force open the collapsed airway. The net effect is awakening, every 2-5 minutes, all night long. Guess who well rested that person feels the next day! If you have an issue of fatigue, and you snore, you likely have some measure of sleep apnea and are not getting restorative, restful sleep. (Mild sleep apnea = 5-15 episodes per hour, moderate is 15-30, severe > 30)

It is intuitively obvious that extra weight makes sleep apnea worse. The need for effortless, easy breathing is impaired by extra weight on the chest and abdomen. The diaphragm has more work to do. There is more weight in the neck area. Extra fat provides less room for muscles to move it. But it has never been studied as a means to cure.   This is the first study looking at weight loss as the solution.

That’s what this study provides. For the first time, obese men and women were taken and carefully instructed to make meaningful life style changes so that real weight could be lost.   They started with 81 subjects, and finished with 47.   They all had sleep apnea. They were followed for 5 years while being counseled. Those who achieved 5% weight loss were considered successful (n=20) versus those that didn’t achieve meaningful weight loss. (n=27) The risk of progression to more severe sleep apnea was reduced by 80% in the weight loss group compared to the other group.   Some men were cured completely. The dietary intervention was to increase the consumption of lean meats, fish, fruit and vegetables and to avoid desserts, dairy fats and saturated fat. (No wonder only 20 men lost weight.)   Exercise was counted when men exercised 30 minutes three times a week.

The main finding, that sleep apnea gets better with weight loss, is huge. But this is a very small study, and only a tiny bit more than 50% could finish it. An 80% reduction of progression when you have only 20 participants might be a very small number. What is more interesting to me is that they found 20 folks who could lose 5% weight on a low fat diet. We now know that these folks will fail in time and regain their weight. The only weight loss that is long lasting and successful has the consumption of fat as central to its mechanisms. Eating carbs turns on insulin and insulin stores calories: that’s how you gain weight.

WWW. What will work for me. I think it’s time to take this knowledge and press the advantage. In my practice, I have dozens of folks in just a few years who have dramatically improved their weight, and sleep, and very likely their snoring. We don’t need more studies of low fat weight loss, we need a high-fat, low carb (>20 grams/day) weight loss study. That will show folks to be cured.

Pop Quiz

  1. Sleep apnea can be cured with 5% weight loss? T or F


  1. This cure applies to men and women. T or F


  1. Snoring is a cardinal symptom of sleep apnea. T or F


  1. Sleep apnea will get worse over time if you don’t lose weight. T or F


  1. Sleep apnea is a huge risk for heart attack, diabetes, high blood pressure. T or F