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Connexins and Diabetes

Connexins and Diabetes

References: J. Cell Biology, J Biol Chemistry, FEBS Letter,

Connexins. What we learned last week was basic. Connexins are the proteins that make for connections between cells. They exist in every creature with more than a few cells. For multicellular organisms to exist, connexins have to become part of the picture. And the management of fuel for cells in central to an organism that has specialized digestive processes. To have a gut, blood, central nervous system, bones, muscles and everything else means you have to have a centralized control system for fuel allocation. That central traffic cop is the pancreas gland with its beta cells. They produce insulin, and insulin is the key hormone used to signal storage of calories for future use. Traditional medicine calls insulin your blood sugar controlling hormone. A more inclusive vision would be to say that insulin rises in response to rising blood sugars which occurs during the time of year of calorie excess, just before the time of year of calorie deficit. It’s a good time to store calories.

The storing of calories as insurance against future starvation is a key feature of human survival (and all creatures). That’s insulin’s job. How do connexins play a part in all that? These articles this month go right to the heart of that role. When you knock out the ability of pancreas beta cells to make connexins, their ability to make insulin drops proportionately. This means for us to have a sensible, balanced and nuanced control of glucose, we have to have proper connexin function.

What happens in humans when we get overweight, and become diabetic? Our fat cells get bigger and we demand more and more insulin to keep glucose in a tight range. We can produce that extra insulin for a while, but eventually exhaust our ability to produce sufficient insulin to control blood glucose adequately enough. Glucose is a very reactive chemical. Granted, it is fuel to burn, which is why being reactive helps, but high levels of it stick to all sorts of places where it’s not meant to be. And that leads to disease too. Our body doesn’t like high glucose, and we frantically put out more insulin to regulate that. And what happens when we can’t make enough insulin any more? You got it, the first step is connexons between cells dropping off as we produce fewer and fewer connexins. This makes connexin dysfunction the first step in diabetes development. The ability of our beta cells in our pancreas to talk to each other via their connecting connexins is the first step to developing diabetes.

And guess what happens in heart disease, brain disease, muscle disease, kidney disease?…..Name an organ and I can show you references that demonstrate that connexins fall off and connexons (the name for the actual channel between cells) between cells decrease. The level to which all your organ types are connected to each other is the level to which you are healthy. This loss of intracellular connections via these proteins called connexins is the basis of much illness.

The $ 64 k question is, what can we do to alter our connexins? Is that something we have control over? And the answer is yes! Next week.

www.What will work for me. All right. I’ve learned that connexins are the protein channels between cells that allow communications between similar cell types, allowing different cells to act as coordinated organs. Muscles can contract together. Liver cells and digest together. Brains can think… etc. Sounds like this is at the heart of life of multicellular organs. I love getting down to the very basic facts. But I’m eager to know how I can alter it with my own behavior. I guess for that, I have to wait till next week.


Pop Quiz:

‪1. Connexins are the key mechanisms of different cell type to function as independent organs. T or F

Right on.

‪2. In diabetes, our pancreas beta cells have more connexins functioning with higher blood glucose. T or F

False.     That’s backwards.

‪3. Virtually every illness with organ dysfunction can demonstrate lousy connexins of the organ that’s not working. T or F

T.  Isn’t that fascinating?

‪4. Earth worms have connexins. T or F

True. They have muscles that work in a coordinated fashion. That wouldn’t happen without those links.

‪5. Our gut has connexins that get discombobulated with gluten. T or F

Bingo. You intuited that and you were right. Gluten disrupts connexins between gut cells.


How to Make a sdLDL (Small Dense LDL)

How to Make an sdLDL (Small Dense LDL)

References: Lecture by Ron Rosendale, Researchgate, PLOS, JCI,

This is the most common question I get asked: what do I do when my doctor wants to put me on a statin? It gets asked by healthy folks who have all data they need to prove that they don’t need a statin. They are eating optimally and their lipids are, in fact, beautiful. But their doctor thinks they should be on a statin because the rules for cholesterol treatment have been dumbed down to the barest essentials: is your cholesterol over 200? Statin!

Repeatedly, I go through the exercise of explaining that it’s not the total cholesterol that matters, it’s the number and size of particles that matter. If you have big, fluffy LDLs, you are in great shape. If you have small, dense LDLs, you are in big doo-doo. The proper analogy has come down to asking which has more volume, a pick up truck bed or a 5 gallon bucket. (Hint, it’s the truck.) And how many basketballs can you put in a pickup truck? I usually hear “About 50.” And how many golf balls can you put in a five gallon bucket? I hear 400-500. This is as close to your cholesterol as I can get. You don’t need a statin to treat basketballs, they are harmless. They are the equivalent to big, fluffy LDLs. And you don’t need a statin to treat sdLDLs either, unless you can’t change your lifestyle. But your doctor is unlikely to know how you make sdLDLs (golf balls) so they can’t advise you how to do it differently by lifestyle. Besides, a pill is easier and faster and you get to bare the side effects and consequences, but not much benefit from taking a statin.

Ok. The nugget comes down to, “How can I change my small, dense LDLs to big fluffies?” That’s the nugget. And the answer is ….. get rid of insulin. This will save your life. Get rid of insulin. How do I know that? And vice versa: How do I make small dense LDLs? Turn on insulin.

SdLDLs are made in response to insulin. Insulin is made in response to carbohydrates overwhelming your ability to burn glucose. You are signaling your body that you are in the season of carbohydrate excess. That’s fall when plants ripen. You are gorging on carbs. Winter is coming. You need to get fat. You want insulin to make a lot of different actions. You need to increase the production of fat in your liver. Those are called triglycerides. You need to make more transport modules to move the fat from your liver to your fat cells. Those transport modules are called LDLs. But because you have to make oodles of them very quickly, you make small ones just to get them off the production line. And as your fat cells get bigger, they become insulin resistant as the insulin receptors get further apart on the expanding fat cell. Your insulin level rises. You have insulin around all the time, and presto, you have small dense LDLs.

Want to make your LDLs bigger, safer, kinder and gentler? Sure. Then get rid of insulin. Stop eating carbs, and stop eating too much protein. That leaves fat and very low glycemic carbs. (Above ground vegetables) Your LDLs deliver their product, turn into HDLs and you can watch your LDLs drop like a rock and your HDLs climb steadily – about 5-8 points a month. Get your carbs below 20 grams a day and your HDLs will reach 100 in about a year.

WWW. What will work for me. It’s that simple. You can prove it in weeks if you have a lab that will order your HDLs, your sdLDLs and your insulin. Get your insulin below 7, and you will be good. My HDLs were 28 all my life until I lowered my carb intake. I’m now in the 60s, and not quite disciplined enough to get higher. I’ve seen this question so many times, I wanted to put it all in a handout I can show my clients. Here it is. Cut the carbs, eat more butter, make your LDLs get big and harmless. Eat cookies, brownies and ice cream and presto, all the sdLDLs you want. And that’s how to make a sdLDL.

Pop Quiz

‪1. Total cholesterol should be below 200. T or F

True if you are the American Heart Association. It doesn’t matter is you are a scientist and want to know truth. The HUNT study from Norway says women live longer if their cholesterol is over 200.

‪2. If total cholesterol isn’t the measure of trouble, what is?

Probably your Triglyceride/HDL ratio or your Apo-B/Apo A2 ratio – both connected to sdLDLs

‪3. I can raise my HDL be eating bacon and eggs? You’re kidding?

Yup and Nope

‪4. There is consensus in literature review that eating saturated fat is harmless for you. T or F

True. Read the review in the American Journal of Clinical Nutrition.

‪5. sdLDLs are the ones that cause heart disease? T or F


How We Have Been Deceived About Sugar

How We Have Been Deceived About Sugar

References:  New York TimesInt Jr of Health SrvWashington PostGary Taubes in The Case Against Sugar  Huffington Post,

Just about every mammal loves sugar. Of course we do. Through most of human history, it meant ripe fruit becoming available, just before the long dry season of either African drought or Asian/European cold. But in the last 200 years, sugar has become even more bountiful. Sugar was such a hot item, Arabs made a killing transporting it over deserts to Europe by camals. Columbus was all about finding places to grow sugar in the New World, as were all the European colonizers. The Caribbean was hot property, because of sugar. Our biology naturally drives us to seek sugar. Plain and simple.

What we haven’t understood is the power of political money and “lobbying” to undermine our scientific process of enquiry. In America, our politicians carefully guard their re-election money sources, and don’t reveal it, but it is a pay for play game. And this game has been going on for almost 70 years before it has started to come unraveled. And you play a part in it, because you love sugar. You and I both eat more food with sugar in it, and that rewards food companies to add sugar to everything. In fact, Lustig, one of America’s premier sugar adversaries, has documented that 75% of all American foods have sugaradded. And with your consent, the sugar lobby has been focused, nefarious, diligent and successful. It has paid off politician after politician to intercede in just about every guideline every issued about food, to change the conversation with little phrases that shift the truth in a way that just isn’t so. When the World Health Organization, a group outside the USA, tried to issue guidelines limiting sugar to just 10% of calories, the sugar lobby went crazy and got Senators to threaten to pull all funding from the WHO if those guidelines went through.

But it’s worse than that. The shifting of blame to fat was the real win. We have spent decades fighting cholesterol, making a huge artificial industry about statins all because a few key American health leaders, paid off by the sugar industry, pushed us that way. Today, you can still see that effect when you go to the store and buy LOW FAT Yogurt, as though that was a good thing. Please, translate that LOW FAT label in your brain to be HIGH SUGAR, because that is the net effect. And you slurp it down happily. And you can see your waistline, gradually expanding. And all along, it was sugar to blame.

The proof is finally falling together. Metabolic syndrome, the underlying driver of heart disease, cholesterol, hypertension are each and collectively more tightly linked to sugar than anything else. Let me repeat that. Sugar, not fat is the core enemy. You obsess about cholesterol to your peril. It’s sugar.

And what does the sugar industry say to that? Same old play book. Deny, shift blame, “Calorie is a calorie”, “Obesity is all about poor food choices and eating too much”, and other stock phrases are all intended to deceive. And you go down.

The final deceit are all the alternative names for sugar. There are SIXTY ONEcurrent names out there on food labels for sugar. And we are not always as clever as we think when we go for agave, barley malt, cane juice, mannose, maltol, maltodextrin, Desmara sugar and some 50 other names for sugar. You will typically find 3-5 of them on any “healthy” snack bar, which in total makes sugar the number one ingredient in the bar.

Is there an amount of sugar you can safely eat? Well, not really. We are currently around 82 grams a day and close to 10-15 % of our calories from sugar. But many of us are getting more than that, and are sicker to show for it. The American Heart Association says to get down to One Ounce (100 calories) a day for women, for about a 75% reduction. (150 calories for men). If you have high blood pressure, diabetes, are overweight, have elevated bad cholesterol, worried about Alzheimer’s, heart attacks or anything else, less would be better. Generally, any reduction, at any point, is better.

WWW. What will work for me. I’m having fun looking at all the goofy names for sugar on different packaged foods. They are out there. I’ve trained myself to see LOW FAT as HIGH SUGAR. And when I get off sugar and stay there, my HDLs start climbing. I’m back up to over 60 again. You could be there too.

Pop Quiz

1.  Panocha and Muscovado are safe sweeteners. T or F


2. Ok, how about Fruit Juice Concentrate? Safe ?
Double sucker

3. The Sugar Industry Lobby group will happily show you their lobbying dollars paid to your congressman. T or F
Wow, you really are trusting. No. But just about every congressman gets some.  Rubio and Sanders.
4. US Senators threatened the WHO with withdrawal of funding if they didn’t change their recommendations on sugar, lowering its use. T or F
You can simply always vote for the worst option. That would be true.
5. I can safely eat sugar and not damage myself. T or F
False. At 15% of calories, you will have metabolic syndrome within a month. Longer at lower levels. How long do you want to stay well?

Eat Chilies, Live Longer

Eat Chilies, Live Longer!

Reference: PLOS 1, Medical News Today, BMJ,

Whoo Hoo! I get to eat chilies and hot sauce and live longer to boot. Isn’t that a bit of fun to cheer up your gloomy January morning? Show me the proof.

That’s what this study reveals, released just this week in the on line journal PLOS 1. The authors from the University of Vermont took a sample of elder Americans over age 18 from our national nutrition survey called, NHANES, and followed them for 18 years. 16,179 carefully randomized Americans, followed for 18 plus years end up being 273,877 human years of follow-up with 4,946 deaths. You are getting to large enough numbers for the ability of statistical analysis to be meaningful and true. The risk reduction of death was from 33.6 percent for “non-consumers” to 21.6% for chili-eaters. That’s an absolute risk reduction of 12% or a relative risk reduction of 36% stated as an RR of .64. That’s a lot.

Pretty good? Huh! So, how? A prior study in the British Medical Journal, found the same thing. It was much, much bigger, but in China, not America. The Chinese eat some seriously spicy food. In that study, 199,293 men and 288,082 women were followed for a total of 3,500,004 years. They asked how many days a week spicy food was eaten, and found that adding a day added an increment of reduction, for a relative risk reduction of 14%. Their findings were also statistically significant. Again, they noticed a reduction on cardiovascular mortality.

Again, how? There may be many mechanisms. We know that populations who eat more chilies have less cancer. Capsaicin is known to disrupt the cell cycle and has been advocated as an anti-cancer drug in the form of a product called Capsol T. The ability of capsaicin to reduce lipids has also been documented. The antioxidant effect of capsaicin is well known. It has been found to alter the biome in the gut.

Goodness, gracious. Chilies are good for you. One day a week is good, two is better, seven is best. One of the articles suggested that part of why chilies may be good for you is that you eat less, you are satisfied faster. Hmmm. Perhaps because you are frantically fanning your mouth and pushing your plate away. What ever works!

WWW. What will work for me. I have used Capsol T in my practice. It is a combination of green tea and chilies, and when used every 4 hours arrests the cell cycle in cancer. But I also have chili sauce on my dining room table. For Christmas I was given Ghost Chilies as a condiment and I have been putting one flake on my eggs in the morning. Now, after 4 weeks, I’m up to 4-5 flakes. And I must admit, I love it. It’s a new flavor that is tasty and delightful. It makes my three egg breakfast something I look forward too. Building up slowly might be the way to go.


Pop Quiz

1. Eating chilies daily will lengthen my life. T of F

Possibly. Population studies aren’t quite generalizable, because you may not be one of the ones who benefits, but the population you are in will. 13% less mortality.

2. The benefits of eating chilies come from cardiovascular risk reduction. T or F

Partially true again. We aren’t sure of exactly what the mechanism is. It appears to be multifactorial, meaning we still can’t put a finger on it.


‪3. The hottest chili in the world is the Ghost Chili? T or F


Well, actually false. The Hottest Chili is now the Carolina Reaper, a hybrid of the Ghost Chili from Assam, India and a Habanero bred at the Puckerbutt Pepper Company.


‪4. You should start eating chilies today. T or F


Well, true on general principles but it’s pretty clear it takes a while to get your body used to it. Starting low and going slow is likely the way to go.


‪5. Chilies came to us from the New World in Ecuador, and spread all around the world. T or F


False. Mexico, but close enough. Now, the most chilies in the world are grown in India,

Prolactin, A Problem for Older Guys

Prolactin, A Problem for Older Guys

References: Jr of Endocrinology, Wikipedia, Nature Reviews,

Ever heard of prolactin? Bet not. From its name, you can surmise that it has something to do with helping lactation: “pro” – lactation. And that’s just what it was discovered to do. It is secreted from the anterior pituitary in response to breast stimulation, and helps milk let down. A mother can successfully breast feed when she has her infant stimulate her nipple. That was figured out in the 1970s. Since then, we have found over 300 other functions that in which it participates.

Prolactin isn’t just made in the pituitary. It’s made in lots of other places in much smaller amounts. It is quite similar in structure to growth hormone, nature being efficient with hormone design and building off one hormone to make more functions. It has 198 amino acids in it, so is a peptide hormone. As we dig deeper into biology, we are finding that the human metabolism is far more complicated than anything we ever imagined. Orgel’s Third Law alludes to that: Nature is more complicated than you imagine, even when you take Orgel’s Third Law into account.

Now, here’s the rub. One of it’s functions is men’s refractory period. The refractory period is the time after an orgasm during which a man is unable to be aroused again, cannot achieve an erection, and would rather read a book. That period is usually short in teen years (5 minutes) but gradually lengthens with age. With the right environment, it might only be a few minutes – hours in the 20-3os. By the age of 50-60, it can be a few days. Prolactin appears to be the mediator of that refractory period. As men age, their prostate gland enlarges, and the prostate also makes prolactin.

That’s where this week’s study comes in. Ten men in Germany, who were otherwise healthy, had their prolactin measured and then shown erotic films and instructed to masturbate. This is hard to turn into a double blind trial, as you can imagine, so it was single blinded and crossed over so that then subjects didn’t know when they were getting a prolactin inhibitory drug called cabergoline. The cabergoline arm of the study was found to have significant reductions in prolactin, and enhanced of all parameters of sexual drive (<0.05), function (<0.01) , and perception of length of the refractory period (< 0.01). The authors suggest that this is a possible route for study as we look into future effects on men’s sexual health.

Prolactin has over 300 actions in the body. It may play a role in brain cells making myelin, it probably mediates women’s infertility while breast feeding, in infants making surfactant in their lung, in immune tolerance of the mother’s immune system to the fetus, the production of new brain cells… Orgel had it right. Nature is complicated, and we are just unpacking the surface. The interplay still to be discovered has a way to go.

WWW. What will work for me. Well, it turns out cabergoline is now a drug on the market used for men’s sexual health called Dostinex. And we are finding the measurement of prolactin starting to seep into standard blood assays. In my practice, my most used blood panel has it as a newly added feature, and I’m finding a lot of men and women have modestly elevated levels. I tell folks that a tiny percentage may have a pituitary tumor, but what to do with slightly elevated levels is still uncertain. There are web sites on how to lower it naturally for both men and women.

Pop Quiz

‪1. Prolactin is a hormone that helps women breast feed their infants. T or F T.

That is what it was discovered to do

‪2. Elevated prolactin plays a roll in some men who have sexual dysfunction. T or F

Again, true.

‪3. Prolactin is secreted at the end of a sexual encounter and accounts for the sense of satisfaction afterwards and the inability to become aroused again. T or F


‪4. It is easy to measure prolactin. T or F

‪It is almost becoming routine, and lots of folks have modestly elevated levels.

‪5. Prolactin causes cancer. T or F

Whoa Nellie. Not so fast. It may be a growth factor for some cells, and cancers tend so shop around and find what growth factors they can use. Prolactin is similar in structure to growth hormone, but it isn’t really a cancer causer.

Hormone Replacement with Estrogen Improves Lung Function

Hormone Replacement with Estrogen Improves Lung Function

References: Pro Natl Acad of Sci, Townsend Letter, Menopause,

Did you ever wonder how women adapt to being pregnant? One of the key adaptations is that they have to breathe for two, and that’s while their abdomen is being pushed up by the pregnancy. Can’t you imagine breathing enough with a basketball under your belt? This question arises when I see a women who has lung disease. Can we help her adapt to the challenges of that lung disease with hormones? And the answer is yes! This is particularly important because nonsmoking women actually have more chronic lung disease (called COPD) than non-smoking men.

The first research came out in 1995 with the Drs Massaro showing that pregnant rats almost double their oxygen uptake ability. They do it in a unique way. They generate more and smaller alveoli than male rats, (the tiny air sacs where air exchange happens) leading to greater surface area for oxygen to diffuse across. The same researchers then took immature rats and showed that their lungs made many more small alveoli when given artificial estrogen, compared to controls. So, it was estrogen that does it!

Testosterone in the same context didn’t do it. And then, mature rats who had their ovaries removed lost lung surface area and increased the size of their alveoli, all leading to less oxygen capacity.

The authors conclusion was that estrogen plays a key role in lung function in female rats, and can result in regeneration of new and improvement in existing alveoli.

This then lays the table for us to think about humans. The authors wrote a review article on estrogen and women with pulmonary dysfunction. Menopause becomes a critical risk period. With the loss of estrogen, alveoli decline and what may have been adequate prior to menopause because inadequate after. Considering how many women have chronic lung disease without even smoking, this becomes a critically important issue for the safe and optimal care of a post menopausal woman, with any lung disease. The same applies for men. They need some estrogen too, and if their testosterone gets too low, their estrogen conversion doesn’t happen enough to support lung function.

WWW. What will work for me. I’ve always considered estrogen replacement to be critical for brain and bone function. Then we added heart disease, and reduced breast cancer risk. Now, it’s clear that lung function is part of the mix. It only makes sense. What is part of your optimal healthy environment is still part of that combination when menopause arrives and estrogen declines. No wonder women with higher estrogen live longer. No wonder the Leisure Study found that women who use hormone replacement for over 15 years live the longest. I’m adding this to may armamentarium of reasons to be on BHRT.

Pop Quiz

‪1. Pregnant rats demonstrate markedly increase oxygen absorbing capacity. T or F


‪2. Must of this increased capacity in pregnancy comes from smaller and more numerous alveoli? T or F

Again, right on the mark

‪3. Rats with ovaries removed recover more and better alveoli when estrogen is replaced. T or F

You are on a roll. Keep it up

‪4. Humans also get better lung function when they are given estrogen after menopause. T or F

Again, true

‪5. Which makes it obvious that the Leisure Study shows that women live longer when they are on hormone replacement. T or F

Perfect. A good start for the new year.

Leptin, Weight Loss and Carb Nite Out

Leptin and Carb Nite Out

References: The Carb Nite Solution by John Kiefer<- 
, American Jr Physiol Endo Acta,

Ever plateaued on weight loss? You and everyone else. We now know that you don’t lose weight unless you quit carbs and turn off insulin. So far so good. But somewhere along the line, you plateau and stop losing weight. You are frustrated and upset. The method seemed to work for a while and then didn’t.

What’s cooking? The problem is that we are much more complicated than just insulin. In response to every environmental stress you get all sorts of other hormones. Prolonged dieting with starvation is a real stressor. That causes you to release insulin AND cortisol. That grows new fat cells. Then you regain weight above and beyond when you get back to normal eating. And leptin, your hormone that signals sufficient calories, drops to very low very quickly. When leptin is low, it means either that you are at normal weight, or that you are starving and need to conserve calories. When it’s high, you are signaling that your fat cells have enough food and you can stop eating, or you are resistant and have a lousy appetite control. Which is which? We have been concerned those high leptin signals indicating leptin resistance, and abnormal weight leading to confused weight loss signals.

But that’s only on one layer of complexity. Which is it?

John Kiefer has stumbled into the next layer with this book. In his own attempts to lose weight while not losing muscle, he applied his physics research approach to weight loss and found ideas deep in the basic science literature about how to “hack” leptin. He devised his “Carb Nite” method from that and wrote the book. And when a client of mine came in having plateaued and “broken through” and proceeded to lose another 15 pounds, I read the book too.

John Kiefer’s method is actually ingeniously simple. You have to start with very low carbs – have to. That’s baseline. Maximum of 30 grams a day. That’s what we have been teaching for a while. Then, and catch this, you must have a carb night every 7 nights. Must. No skipping. Not more frequently than every 5th night. And for 6 hours, you get to have carbs. Lots of carbs. Two or three hits. Go for it.

What happens is a spike in insulin. All true. But then, also a spike in leptin. Here is the unique part. Your insulin comes down in 8-12 hours, but your leptin stays up for a couple of days. In the environment of weight loss, your higher leptin signals to your body that you have plenty of calories, so keep burning. In animals there is even evidence that you kill off baby fat cells and don’t grow new ones. And the effect lasts a full four days, shadowing the 8-12 hour effect of insulin.

Did you get that? Ok, a repeat. Cut your carbs to less than 30 a day. Go for 10 days to get started, then have a carb night. Not just a donut, two or three good hits of carbohydrates. Have some mashed potatoes, some ice cream, how about pancakes…. I’m serious. Then back to 30 grams max. Repeat once a week once you are started.

WWW. What will work for me. I’m completely on board with this idea, having seen dozens if not more folks who have plateaued and then gotten discouraged. If you are one of those who has gotten stuck, give it a try. Buy the book. Let us know. I believe it and think this is a meaningful advance. I would love to hear anyone’s contrary opinion, and any success stories.


Pop Quiz

‪1. To lose weight, I have to turn off insulin. T or F

True but it only works for a while. Once leptin falls to low levels, your body goes into conservation mode.

‪2. So the key to losing weight is to starve myself with just 1200 calories. T or F

False, false, false. You will fail because you induce huge stress response, and the resultant cortisol peak will make your grow more fat cells than ever, resulting in new weight gain over and above.

‪3. What’s the key physiological change that occurs with Carb Nite?

You reignite leptin to get back to its originally intended signal, that you have sufficient calories and your fat cells can start losing again. That’s leptin’s original role. When you are overweight, it gets too high and for reasons not completely understood, you become leptin resistant and lose that signal.

‪4. The effect of leptin lasts 12 hours and insulin from carb night lasts 48 hours. T or F False?

Backwards and wrong numbers. The insulin lasts 8-12 hours but the resurgent leptin will be ignited for at least 4 days. Think of it as 1 step back but 4 steps forward. But forward it is.

‪5. You have to have at least a candy bar on carb nite. T or F

False. That wouldn’t be enough. Probably at least two good insulin peaks a couple of hours apart. (Isn’t that fun? Icecream and then more later!)

Soccer Headers Cause Memory Loss

Headers in Soccer Cause Instant Damage to Memory

Reference: eBiomedicine Oct 2016, BBC News, Washington Post,

You have certainly heard of all the controversy about concussion in the NFL. And you likely have heard that American youth soccer’s governing bodies have banned headers for anyone under 11, both in practice and in play. The question remains, are headers a problem for those older than eleven? That’s what this study decided to look at.

The design was pretty simple. Young adults, ages 19-25, 14 men and 5 women, were told to perform 20 headers over 10 minutes from an automatic soccer “gun” that was designed to send the ball at a precise speed, similar to a corner kick. Then they were checked for memory ability; before, immediately after and for 24 hours following. All had measurable memory loss. Some of the subjects had error rates increase by as much as 64%. It seemed to all clear after 24 hours. A recent review of the issue from March of this year suggests this is a problem. Soccer is the world’s most popular sport, and the header is a critical part of the current game.

So, I thought I would share with your my research on concussions and prevention. As some of you may know, I have applied for and been granted 5 different patents on the use of “air cells” in helmets to reduce concussive injury. I have spent the last two years making a testing device and developing a series of experiments to show the effectiveness of air cells. There are some serious barriers to making it work, which is why I’ve taken two years at this project, to date. But we finally have air cells that are tough enough to not pop when I jump and down on them (210 pounds). My testing device can go up to 150 gs in force, at which point they do pop. So, I can deliver great force. And what I find is that the concussive force occurs in the first blink of an eye, .001 seconds. It’s the same principle with your phone. When you drop it on concrete, the glass shatters from a force wave in the first .0001 seconds. If you put a dumb piece of rubber around your phone, it just bounces.

When you put the air cells in my testing device, we find that we fall below the “threshold” to even get the data recorder to start. The decrease in G forces is on the order of 80 to 90%. I need to have a threshold of G forces to set off the accelerometer, and when it drops below 3 gs, the machine fires off when you start it from the acceleration, instead of waiting for the deceleration. Nice problem, huh?

I think there is air under these wings. This idea has got credibility. We can reduce concussive force in sports. It is going to take the design and manufacture of new new protective equipment to do it.

WWW. What will work for me. I’m just starting the process of looking for business development help. License it? Make it? Prototype it? I think all sports helmets needs to change. Tough resilient air cells will do it. There are other methods. I’m working on a baseball cap right now, with a layer of air cells in it. I whacked my head today in the garage as I was getting put the snow thrower from the crawl space. If I had had my protective, air cell cap on, I wouldn’t have dinged my brain. Now, I just have to remember how to mail out this email.

Pop Quiz:

‪1. Headers in soccer cause brain damage? T or F

That would be a yes.

‪2. Modest head impacts can also cause change in brain function. T or F

That’s what this study shows here.

‪3. The damage appears to occur in the first .001 second when deceleration reaches its peak. T or F

That is the same effect as you dropping your smart phone on the concrete. If you have a rubber cover, it doesn’t shatter. If you don’t, well, you know that story.

‪4. Air cells save lives in what other event where deceleration causes dangerous damage? (Hint: 35 mph will kill you.)

We call them air bags in cars, and they have revolutionized auto safety, if they don’t kill you with shrapnel

‪5. Moderate impacts appear to clear damage within 24 hours? T or F

That is now considered true. What we do know is that repeat concussions within the first week are much more dangerous, so the damage may not be completely cleared in 24. It may take at least a week for the whole healing process to be completed. And we are now discovering and linking repeated head injuries with later-in-life neurological disease. So many little injuries may not be safe.

Vitamin K2 Builds Stronger Bones

Vitamin K2 Builds Stronger Bones

Reference: European Jr of Endocrinology    Published Nov 21, 2016

Vitamin K2 is going to be the story of the decade when it comes to bone health. Why? Well, hip fracture is currently happening at a rate of 17% of elderly Caucasian women and 6% of Caucasian men. African Americans are lucky, breaking their hips much less frequently than Caucasian women. But the incidence of osteoporosis is increasing around the world with rates dramatically rising in countries where doubling and tripling of rates of fracture in the last few decades is not uncommon. And hip fracture is not safe for you! It dramatically increases your mortality in the following 12 months with as many as a third of folks never escaping hospitals or chronic care facilities after their fractures.

Kids need K2 also. You reach maximum bone density around age 20-25 and that predicts what will happen to you over your remaining 60 years. Did you know that the rate of forearm fracture in kids has increased from 262 / 100,000 in 1969 to 399.8 in 1999? And lots of evidence aligns that with the loss of K2 in our diet, and our kids’ diets.

What’s happening? My interpretation is that around the world we are industrializing our food supply, raising our animals on feedlots. In that context, they are losing grass as a food source, and consequently losing their source of Vitamin K which they change into K2. When we humans eat those animals, or their milk products, we don’t get K2.

And that’s why I believe this article this week ought to raise eyebrows. In this study, 148 postmenopausal women who already had osteopenia were given Vitamin K2. It was randomized, placebo controlled in methodology, so should be valid. And the results were simple and significant. K2 prevented the loss of trabecular bone compared to the placebo group. This is the first study I’ve seen in which Uncarboxylated Osteocalcin was measured and was proven to decrease (that’s good) by 65%. You want your osteocalcin to be carboxylated as then it is able to bind calcium into bone. This validates the COMB study in which 77 volunteers increased bone density in just one year by 2-4 times the amount of those taking bisphonates. The COMB study wasn’t randomized. They were volunteers. So, it’s been questioned.

I’ve had a tricky time finding what happens to food when animals are moved from pasture to feedlot. I remember one reference that compared Gouda cheese from America to Dutch gouda and saw a 90% difference. But I can’t provide that reference. There is lots of evidencethat the bacteria that make gouda actually make K2 themselves. This makes gouda a very good source of K2.

Can you get enough K2 in your diet today? Well, no. To get 45 mcg, the minimum you should have a day, you would need to eat 5 Liters of yogurt, 8 eggs, 5 liters of milk and 8 pounds of beef. Not practical. If your meat is grass raised, well, better. We just don’t know how much.

If you look at guidelines for preventing hip fracture and osteoporosis, you don’t see mention of K2 yet. It should be there. If you know it, you are ahead of national guidelines. Now that we can measure uncarboxylated osteocalcin, it will soon become apparent and it will become part of our annual examination.

www.What Will Work for Me. I think K2 is a critical nutrient that every human should be on. We used to get it when we ate grass raised animals. Back when we were hunter gatherers, or primitive farmers, that was easy. It isn’t easy now. But one in six of us breaking a hip should give us pause and passion. Use that passion to buy some gouda cheese, and take K2 for the rest of your life. Think of the investment in you that makes. Ask your doctor to order your uncarboxylated osteocalcin. (Have a sense of humor…..they will look at you like you were a little daft.)

Pop Quiz

‪1. My risk of breaking a hip is?

‪Women 17%, Men 6%, African American Less, Asian in Asia, Less

‪2. If I take K2 I can expect my osteocalcin to become decarboxylated. T or F

False. It becomes carboxylated, and that is what actives it. Simple put, it completes the basket that holds calcium tightly. Without K2, you can’t hold calcium tightly.

‪3. This weeks study has validity because? It was a randomized, placebo controlled study. Nice work

‪4. The COMB study showed that folks decreased their risk of hip fracture? T or F

False. That wasn’t proven. But their bone density increased up to 8% within one year. And in my practice, I’ve seen several folks hit 7% with a year.

‪5. K2 is widely appreciated in national guidelines. T or F

Not yet. Hardly made a peep.

Statins Lower Men’s Testosterone

Statins Lower Men’s Testosterone

Reference: Pubmed (Endokrynol Pol),  Wikipedia,

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I’ve known this for years. You probably have too. I just wanted to read about it and get it in my data base so that I can refer to it freely. I see so many men who come to me with fatigue, lack of “oomph” (initiative), sexual dysfunction, and most of all, fear of cognitive decline. The topic keeps arising and in my practice, I’m now so convinced about men feeling better with sufficient testosterone, I wanted to explore the precise mechanisms of statin damage and just why so many men are on them.

Statins are effective at reducing mortality AFTER a cardiac event. They are one of the world’s most commonly used medications. Virtually every primary doctor has “guidelines” that require instituting statin therapy when certain thresholds of cholesterol are achieved. They haven’t been proven to have a sufficiently large effect BEFORE, if you take into account their side effects and factor in the cost benefit of those. The argument we have is that you can get the same effect of statins by ridding your diet of high glycemic carbohydrates. More on this later.

This study looked at 237 men on statins in Poland. They found that total testosterone declined from 16.35 nmol/L, to 14.9 ( p = 0.008), free testosterone from 39 to 32 pgms (p < .004), and calculated free from .36 to .32 ngms compared to aged matched controls. It looks like this averages to between 10-20% decline.

It makes complete sense. The mechanism of statin inhibition is the blocking of the HMG-CoA reductase step in the production of cholesterol. Making cholesterol is the first step in the cascade of hormone production. Now, here is where my beef with this strategy comes in. This is a very blunt tool. There are a boatload of other hormones you make that follow the first step. For example, step 2 in the hormone cascade is the production of sex hormones Pregnanolone. That’s your hormone of MEMORY. Some argue that it does, and some that it doesn’t. But then, the cascade of hormones progresses down to cortisol in one pathway, and DHEA, estrogen and testosterone on the other side. There are studies that show it has no impact on hormones or gonadotropins. My question would be to ask who funded those studies. I’m skeptical until I see research not funded by pharma.

But the real issue is to explore how to reduce “bad” cholesterol and raise HDL by lifestyle changes. After all, that should be the first step anyways. And this is the dilemma we find ourselves in today. You are told to ask your doctor about how to do healthy lifestyle changes, and then told to eat lots of fresh fruit and vegetables. But doctors haven’t been trained in nutrition.

I’ve been stunned by the changes my clients make with their cholesterol when they avoid high glycemic carbs. That means all grains, potatoes, almost all fruits. Their bad cholesterol gets better, (small dense LDLs), their good cholesterol gets better, (Big fluffy LDLs and Big fluffy HDLs). And we can prove this with lab tests within weeks. One by one. What you eat can change your bad cholesterol to good, within weeks. Try it.

And back to testosterone. Men with lower testosterone have higher risk of Alzheimer’s. And their muscles ache. I believe the incidence of muscle damage is underreported because most studies have wash in periods where people with complaints and symptoms are excluded.

You decide. What risk do you want? Want heart disease, or brain disease? You can have neither is you reduce your grains and high glycemic foods.

WWW.What will work for me. Bit by bit we are finding more salads and stews that are made with vegetables and dark green leafy stuff. That includes an occasional dandelion lead or two. And stop being so panicked about the fat.

Pop Quiz

‪1. Testosterone is lowered by taking statins. T or F

True. Plain and simple.

‪2. There are other side effects from statins including such things as muscle aches and memory loss. T or F


‪3. It takes a long time to make those changes. T or F

False if you can change quickly. Many of us take a while to actually develop new habits. And our lizard brains keep gobbling sugar when ever it gets within reach.

‪4. What is your greatest fear of late life morbidity?                 You tell me.

‪5. I trust the literature published to date on side effects of statins. T or F

If you said true, I have a 40 acre plot of great family vacation camping woods down in Louisiana I would like to sell you.