The Eight Demons of Eating Fast Food: Number 1 is Glycation

The Eight Metabolic Problems of Processed Foods: #1 Glycation

Robert Lustig's new book, Metabolical, is a tour de force. Read it, if you can take the time. Re-read some of its chapters. He clarifies the core metabolic problems that are literally killing us sooner than we should, all because of food being too processed. Here is the first item on his list of the "Eight Metabolic Processes" made worse by modern food.

1. Glycation. That is the glucose molecule sticking to stuff. If it sticks to a protein, it is called the Maillard reaction and is the fundamental driving engine of wrinkles, cataracts, and aging in general. This is sort of like basting your arteries with sweet barbeque sauce. Your arteries get stiffer, your joints weaken, you get old. Your immune system thinks you have an invader and goes nuts. Glycation is what makes diabetes kill you sooner. If the glucose happens to stick to a protein, it's called the Maillard reaction. It's basically metabolic rusting out.

The higher your blood glucose, the more glycation happens. High glucose is a problem but fructose drives the Maillard reaction 7 times faster than glucose. And fructose generates 100 times more free oxygen radicals. Now, a specific breakdown product of fructose called methylglyoxal drives the Maillard reaction 250 times faster than glucose. Where do we get extra glucose/fructose from? A little here and a little there, but 80% of American foods have extra sugar added to them. Modern food has a lot extra sugar added to it because you eat more when you taste real sugar. Table sugar is half glucose and half fructose. Sugared sodas have an even high proportion of fructose (typically 55% fructose) in the form of high fructose corn syrup.


Can you measure the Maillard reaction? Not really easily. You can measure the amount of glucose in your blood, averaged over the last 100 days. That is the Hemoglobin A1c. That number reflects the percentage of hemoglobin molecules with a glucose stuck on them. The definition of diabetes is now an A1c of 6.4 and above. A better definition of optimal health by the Institute of Medicine calls for an A1c below 5.7. Bredesen, our hero for cognitive decline prevention, advocates for 5.5 and below.

If the natural cleaning up processes of your body aren't working effectively, your tagged proteins with fructose or glucose on them start to accumulate and we called the Advanced Glycation End Products or AGEs. The more AGEs you have, the higher the rate of vascular disease and death.

How do you slow glycation down? Easy-peasy. It all relates to the amount of time your body is exposed to higher levels of glucose. (and or fructose). And that is fundamentally related not just to sugars but "processing in general. Let's give one simple example: oats. Completely unprocessed, whole oat grains are coated with an impervious fiber coating that your digestive enzymes can't penetrate. It takes an hour to cook and then some chewing before you swallow because of their natural fiber which keeping your digestive enzymes away from the carbohydrate inside. That slows digestion down, making the glycemic index around 19, meaning a whole grain oat cereal will raise your blood glucose at only 19% of the rate of pure glucose. You can't even find "whole grain" oats unless you go to the feed store. Now, if you crack that whole grain in half and expose an open face of stored carbohydrate to be available to digestive enzymes, the glycemic index becomes 53. It cooks faster too. 

What happens if you roll it and smash it out? That's more "processing". You expose more surface area for digestion. Glycemic index 59. It's rising with more processing. What happens if you smash it to smithereens under high-pressure steel rollers?  Put it in a small aluminum envelope with 4 fake blueberries.  Your glycemic index hits 83.  Almost as good as pure sugar. What we are doing by processing is making the food called oats easier to cook, easier to prepare, easier to eat and...and...and subsequently bad for you. Your blood glucose rises faster. You glycate more.  To add insult to injury, you then advertise that oats are good for you as part of a whole diet.  Nonsense.  Utter, nonsense.  

The devil is in the details. You want WHOLE oats meaning you have to see the grain in its full form. Not "make FROM oats" but "made OF" whole oats. Every food processor wants to trick you into thinking you are getting all the goodness of the whole grain by getting all the ingredients with the fiber and germ all ground up for you. And there is some teeny benefit to getting those vitamins and fiber. But that benefit turns out to be vastly overpowered and negated by the increased glycemic index. (We can go down the rabbit whole of same issue with glycemic load. It's the same argument.)

Now, the final insult is that your digestive system and enzymes and hormones were designed for whole grains. Your blood sugar is meant to rise slowly for a long time to match the length of time insulin lasts. Insulin lasts some 6-8 hours. What happens if you eat refined, powered grains in the form of white bread or bagels? Yup. Your insulin shoots up to respond to the rapid rise in blood sugar you get because white bread is so easily digested. And then what happens? Insulin lasts 8 hours but your glucose gets cleared out in 4. You crash with hypoglycemia and get starving hungry. Hypoglycemia is the net effect of the insulin/refined grains mismatch. You get on that treadmill and you can't get off.

Glycation is wicked. It's enemy number one on Lustig's list. More to follow.

www.What will Work for me. The answer is very simple. Eating for your health comes down to avoiding any grain that has been ground into talcum powder before being baked, cooked, fried, boiled. Our bodies were designed to eat whole foods, chewed slowly, minimally cooked. In that context, your blood glucose rises very slowly and your A1c stays low. You don't glycate. My a1c hovers around 5.7-8 all the time unless I'm very disciplined. I'm a borderline diabetic with awful genes. I'm trying not to eat any bread or flour product at all. If I'm in a place where that is awkward, I find Trader Joe's has wonderful Norwegian "Crispbreads" using no wheat with lots of flax seeds, sunflower seeds and oat flakes and big chunks of a few other seeds.

References: Metabolical by Lustig, Aging Clin Exp Res, Harvard Health, Medical News Today, JCEM

Pop Quiz

1. What is glycation? Answer:                                     Glucose sticking to substances all over your body.

2. More glycation happens under what circumstances?                                   Answer: High blood glucose resulting from the rapid digestion of grains turned into flour as fine as talcum powder that is too easily digested. (Or too much glucose or fructose from sugared drinks....or ice cream...or cookies.....)

3. What is the Maillard reaction?                                      Answer: That glucose or fructose sticking to a protein molecule. Your immune system gets nuts over that.

4. How long does the rise of glucose from eating white bread last compared to insulin?                Answer: Eating a slice of white bread will raise your glucose for 2-3 hours. Insulin, once stimulated lasts for 6-8 hours. Bad mismatch.

5. So what happens 4 hours after a meal to someone who has just eaten a lot of white bread?             Answer: They become hypoglycemic and get low blood sugar. Yikes!

A Hot Bath (Sauna) is as Good as Exercise

A Hot Bath is as Good as Exercise

The Romans did it. They built the hot baths at "Bath" 2000 years ago, trying to civilize those feisty Celts. Queen Victoria took a dip. The Japanese do it. The Fins won't let you build a house or an apartment without a sauna. American's have hot tubs galore. Is there anything to this idea of a "hot bath" other than hedonic adaptation? Well yes. You feel better when you get out of it, and intuitively, you want to do it again. Are there real health benefits?

Well, yes! And the evidence is accumulating as to the exact mechanisms and physiology. We have reported on the epidemiology of saunas on heart disease. In a study published in JAMA Internal Medicine in 2015 from Finland, 2300 men were followed for 20 years and their sauna use was recorded. Over those 20 years, once-a-week sauna resulted in a 49% death rate, compared with 38% of those going two to three times a week and just 31% of those who went four to seven times a week. Frequent visits to a sauna were also associated with lower death rates from cardiovascular disease and stroke. Now, compare that to the 5 days of life extension you get with taking statins. Hmmm....And that was for only 14 minutes.

The Review article on the physiology of "hot baths" is pretty good. The take-home message is that all the markers of metabolic stress that come out in the "metabolic syndrome" get better with sauna. As they do with exercise. Your blood pressure actually goes up in a hot bath. Your heart rate increases. Your arteries have to stretch and dilate to deliver more blood flow to dump the heat. All those mechanisms are the same as what's going on with exercise, without the exercise. There are even reports diving down to endothelial dysfunction, the core root problem of vascular disease. After the sauna, your blood pressure is down 7/5 mm of Hg. That's as good as a blood pressure pill, without the pill. And the same salutary effect is seen with stroke.

The key takeaway is around the idea of "hormesis" which is essentially the rebound benefit from the temporary stress. Exercise is a stress. You deplete your energy supply and force your mitochondria to use up their ATP and start burning fat. If you push to the point of failure, you are just one molecule of ATP short of collapse. You turn on repair and resilience genes. Acute heat exposure is the same temporary "stressor". The mechanisms all go down to the inner workings of the cell. We now know that endothelial dysfunction in the arteries is the first step of developing vascular disease, our 21st century nemesis. Vascular disease can't get started without plasmalogen deficit. It appears that "hot baths" reverse that.

www.What will Work for me. Isn't this interesting? The Fins are onto something here. They have proven the epidemiology of benefit from saunas and are now leading the way in exploring the physiology so that we get more insight into what's going on and how we can improve on it. The question arises, can we get the same effect with sun-bathing? Again, heat exposure for a brief period of time. Now, we are all distracted by the sunburn and melanomas, but is there a similar "hormesis" effect? With this summer's record-breaking heat, I feel we are all getting our saunas. It's only 14 minutes you need. More is likely a bit better.

References: The Conversation, Int Jr Envir Res Pub HealthJama Internal Medicine, J Hum Hypertension, Neurology,

Pop Quiz

1. How long a sauna do I need to get some measurable benefit? Answer: 14 minutes

2. And just how often do I have to do that? Answer: just like exercise, 4 or more times a week is best, but 1-2 a week is better than none.

3. Compared to statins, how much benefit do I have on vascular disease? Answer: well, statins add 5 days to your life. You reduce heart attack deaths by over a third with saunas. It's apples to oranges comparisons, but it feels like some 10 fold better results.

4. If I sauna and exercise, what happens then? Answer: you will have to arrange for some other way to die than heart disease, at some later date.

5. How do I get a sauna? Answer: You can buy one for your home for about $ 1800 or so and get a kit to make an infrared sauna.

Could Ivermectin Help End the COVID-19 Pandemic?

Could Ivermectin Help End the COVID Pandemic?

This ivermectin story has actually got legs to it. If you want to take the full dive, listen to Dr. Pierre Kory's full podcast, done June 1. He is one of America's premier pulmonary/critical care doctors on account of having published more studies than anyone else, but also because he was at St. Luke's, Milwaukee, right here in our hometown.

But here is the story. You see if it has credibility.

The story might begin in Peru. COVID was winning! Hospitals were being flooded with COVID patients. Vaccines were not available. Peru started using Ivermectin and fatalities dropped dramatically. They reported this in April this year. In brief summary, their mortality dropped 74% in a month when ivermectin was used, starting about 10 days after they started using ivermectin broadly in multiple provinces. That took bold initiative on the part of public health workers and elected officials.

Or we could look at Africa. Ivermectin has been used widely in Africa to treat river blindness (onchocerciasis), to great success. There are wide swaths of Africa where folks are taking ivermectin weekly to prevent onchocerciasis. Guess what the statisticians tell us about why COVID has not affected Africa like it has the rest of the world? Bingo: the data shows a protective effect despite the huge challenges of measuring COVID in poverty-ravaged areas. Taking ivermectin appears to be protective against getting COVID.

Take the story of Mexico. In crisis over COVID with its ICU's full, it started using Ivermectin. Test positive and you and everyone in your family get ivermectin, even before you get sick. Mexico's current COVID situation is with ICU beds at 80% empty and the country back on its feet having an election.

There are some 30+ studies. For example, a small study in Egypt at Zagazig University. Of 204 subjects in the treatment, (all had one family member test positive for COVID) only 7.4% developed the disease. The untreated control group had 58% develop the disease. It's a small study, done outside the USA. It was not published in a major US journal. It wasn't randomized, but it did have a control group. Is it valid?

How about India, where it is now being used in some states despite WHO saying not to? But the government of India has now cautiously endorsed its use. COVID in India is exploding because of crowding, poverty, lack of vaccine...they seem to recognize the crisis and the need for decisive new approaches.

You get the idea. We have a world at war with a virus. We have a drug that is cheap, widely available, tiny toxicity profile, long history of safe use and with many studies showing efficacy of one degree or another, and few clinical trials. We know ivermectin has an effect on viruses. There is actually quite a robust literature on it. It works in viruses by "inhibiting recognition of the nuclear localizing... integrase protein by the host heterodimeric importin (IMP) α/β1 complex, and has since been shown to bind directly to IMPα to induce conformational changes that prevent its normal function in mediating nuclear import of key viral and host proteins". Did you get that? But do we have a "large, statistically powered study" to prove it? No, and we never will. It is too cheap. There is no profit incentive and in America, our health care system runs on a corporate profit model, not a public health model.

What is the reason for the silence around using it? What is the "hidden force" behind the scenes preventing our using it? Why don't we have a proper, randomized, placebo-controlled trial being conducted in America, if it shows such promise in multiple places all over the world? Hmmm. You might find Merck's comment instructive. Even WHO is being cautious. The FDA does not appear to be enthusiastic either, specifically stating it is NOT approved for use in humans with COVID.

www.What will Work for me. If I were "in charge", I would make the proper study of ivermectin the highest priority. In a war you need many tools to attack the enemy. And you don't put false arguments out there about "not being studied". In World War II, we never had a randomized, placebo-controlled trial of parachutes prior to D-Day. We just used them after the first demonstration that one worked. They didn't work perfectly, but those early parachutes helped win D-Day and Omaha Beach. My editorial comment is the following. Our health system is sadly broken and focused on profit and shackled by economic interests. This drug is a tool with promise that might serve us well, as part of our armamentarium. I'm writing to my elected officials asking them to please advocate for a study of the drug. You won't get immunity from taking it. That comes only with having the disease, or getting vaccinated. The track record of the vaccine has now been long enough that we can be pretty confident there won't be mystery side effects "sometime in the future". Some side effects would have happened already, and have not been observed. Our elected officials would generate more trust and credibility if they found a way to study this drug instead of stubbornly resisting it.

References: Youtube with Dr Pierre Kory, International Jr Inf Diseases, Inter Jr Good Conscience, SSRN, MedRxIV,

Pop Quiz

1. What is the way to move the needle towards action in America? Answer: all of us writing to our elected officials. Make a politcal noise, peacefully. Please write today.

2. Can you explain how ivermectin works? Answer. Well, its complicated but you can simplify it to say the virus hijacks some proteins. Ivermectin blocks the hijacking.

3. Are you immune to COVID if you take ivermectin? Answer: No. We don't know that yet.

4. If you take ivermectin once a week to prevent river blindness, what are your chances of getting COVID? Answer. Very, very, very low.

5. What is ivermectin used for that is in your home already? Answer: look at the heartworm package for your dog. It might be ivermectin, right in your dog medicine cabinet.

The Mitchondrial Threshold

The Mitochondrial Threshold: The Explanation for All Diseases

How do you explain the root causes of diseases? What is the underlying cause? Let's take a stab at it. See if I can explain to you, in plain enough English the key ideas and have it make sense to you.

It helps to go backwards, so let's make one example: heart disease. A heart attack is actually the final end-product of 30 years of arteries accumulating lipids and small, dense LDLs stuffed full of triglycerides. But what got that started? We call it endothelial dysfunction, of which the very first step is the lining cells of arteries being stressed by too much peroxide. They can't neutralize it faster than it's being made. Peroxide comes from Reactive Oyxgen Species (ROS). (Very elegant research backin the 70s proves it.). So they stop being connected to each other and the artery lining gets leaky. In comes the LDLs. Let's go back another step. What makes the peroxide?

In short, oxidative stress. Now we are back to the mitochondria, our energy factories. Our mitochondria like a regular supply of fuel which they get fed via fatty acid breakdown in the peroxisomes or pyruvate via the glucose pathway. Those are like two separate hoppers, or supply trains, feeding raw energy into the engine. They work best when there is a gradient going downhill all the way through. The very first complex in the electron transport chain is Complex 1 which will push 4 protons into the "reservoir". Now, an active athlete is using up all their ATP in their cells, so the electron transport chain has something to do, a destination for its protons. Ditto for a person who is fasting. Very few protons linger in the "reservoir". The electron transport chain always has an empty slot for the next electron and proton. So, they all get used properly and no reactive oxygen species get pushed out. But what happens to a well-fed, middle class office worker who just had a big breakfast of sugar coated cereal and a luscious coffee purchased on the way to work with 600 more calories of high fructose corn syrup. With little calorie expenditure pulling ATP out of the mitochondria, and both sources of fuel wound up, the electron transport chain backs up. It has more fuel arriving than it can handle and it can't turn anything off. Its only way to cool off is literally to cool off, turn on uncoupling so it makes more heat. But that isn't enough. 

The backing up makes for more reactive oxygen species, (loose electrons that escape complex I and III in the electron transport chain). And that makes for more peroxide. Remember peroxide going out there and damaging your lipids and your endothelium, starting artery disease? It took 40 years for it to turn into a heart attack, but it started sitting in the booster seat in the back of the minivan stuffing your face with french fries and ketchup. They overwhelmed your mitochondria, flooding you with "oxidative stress". The fructose in the ketchup flooded your liver forcing you to make fat. Or in the sugared fruit drink that came in a pouch, or in a donut covered with sugar.

And that is the "Mitochondrial Threshold". Our modern food supply of too much nutrition, of too many kinds of foods, delivered all at once, without any fiber in it to nourish our gut and slow down the delivery of calories. Hence, the cause of all diseases is our modern food supply, delivered with too many purified calories, devoid of any fiber to slow their absorption. We have met the enemy, and it is us.

You can walk through this same scenario with cancer. Dysfunctional mitochondria, with altered internal dynamics pushing nutrients into alternative pathways. In the case of cancer, its citrate being exported into polyamines and feeding cancer.

But underlying all of them is the damage to the mitochondria that overwhelms the mitochondrial ability to repair its own membranes. What is in the mitochondrial membranes that is sucking up and absorbing the reactive oxygen species that gets overwhelmed?


What would happen if you maintained your plasmalogens? Plasmalogens are in place to catch the occasional reactive oxygen species with their precious vinyl ether bond on the outside of the membrane, the only membrane lipid to have such a feature. We deplete them with our modern, highly processed diet. Then, inexorable flooding of our mitochondria leads to mitochondrial dysfunction. Once upon a time we made sufficient plasmalogens to absorb the occasional reactive oxygen. Now, the ensuing flood of ROS leads to chronic disease. That's where diabetes,heart disease, neurodegenerative disease all start. How to repair? 

First! Don't produce so many reactive oxygen species by eating so much highly processed food that floods your mitochondria with too many nutrients all at once, and depleting your plasmalogens. Two, make sure you get the proper nutrients to make sufficient plasmalogens. Understanding how we deplete them and how plasmalogens create a means of measuring our biochemical reserve creates a whole new methodology of gauging susceptibility to chronic disease.

This hypothesis is the nexus of Robert Lustig's brilliant new book Metabolical. Read it. He has a chapter detailing the three great controlling enzymes that get overwhelmed by our eating processed foods. It's sobering and it fits the missing understanding of complexity. And he has a chapter about how to measure where you are. Get the lab.

My addition to this is my understanding Goodenow's contribution that I call the metabolic "shock absorbers" to dysfunction, plasmalogens. His book isn't published yet but this is some of the advanced ideas detailed in it. We can overwhelm our mitochondria in daily living, and our plasmalogens soak up the errors and neutralize the reactive oxygen species. Eventually we wear that reserve down. That's when trouble starts.

www.What will Work for me. Ah, I now understand why intermittent fasting works. You empty out your electron transport chain and allow your mitochondria to get back to running on lean. They like that. I also get how Goodenowe's discovery of plasmalogen absence predicts coming metabolic catastrophe. Their adequate presence means you still have metabolic resilience. They might just be considered your metabolic shock absorbers. The metabolism of fructose fits curiously into the picture as an accelerant, like pouring gasoline on a campfire. Then metformin speeds up your mitochondria to help them clean out. Exercise also gets you to running on lean. What gets you the sickest, fastest? Fast food. Lustig brilliantly simplifies his advice. " Feed the gut, protect the liver". That comes down to more fiber (known as whole food, vegetables and fruit) and less fructose. That comes down to less processed food. Hereafter I'm ordering the GGT enzyme in addition to the AST and ALT so I understand Lustig's lab. I've measured my plasmalogens. I was low. I'm now taking them as a rebuilding plan. My mitochondrial threshold lies in the balance. My brain, my pancreas, my liver, my heart all lay in waiting.

References: Br J Pharm, Nephrology Dial Trans, Atherosclerosis, Metabolical,

Pop Quiz

1. Step one in getting in trouble is? Answer: Per Lustig, what we put in our mouth in the form of highly processed food that gets too many nutrients into our cells too fast.

2. What is Lustig's simple admonition about eating: Answer: Feed the gut, protect the liver. (Aka, more fiber, less sugar)

3. What correlates the best pending vascular disease? Answer: Low plasmalogens.

4. And just what role do plasmalogens play in this whole dance? Answer: They are your metabolic shock absorbers, soaking up excess free oxygen radicals.

5. Can you overcome them? Answer: Have you watched the movie "Supersize Me."? Yes, we all are routinely engaged in that practice with our low fiber, highly refined, western diet choking us with too much sugar.

Statins Add 5 Days to Your Life

Statins Add 5 Days to Your Life

There are cracks in the "statin empire". The $ 18 billion industry has reached out as far as it can possibly go, even to the extent of advocating that virtually all adults should be on statins. But does it make sense and are we really treating a disease or a symptom?

The first crack appeared about 9 years ago around the simplistic rule of 200. Cholesterol above 200, you need statins. Below 200, "You're fine". Well, the Norwegians tested that in 2012 with the HUNT Study and followed some 50,000 folks for 10 years. They found that women with cholesterol over 200 lived longer than under 200. Oops! Is there a problem here? Of course, there is. The real problem is that you get into trouble in your arteries from small, dense LDL particles that have been oxidized. They occupy less volume. You can have a "low" cholesterol and not really be protected. Taking a statin, ironically, reduces the number of large, fluffy, harmless LDLs and not the dangerous small LDLs. That "magic" number of 200 doesn't make sense. It is simply a super easy tool that advertisers and patients can glom onto and believe that sounds like it makes sense. (Statins do have some helpful effect, probably as an anti-inflammatory nature.

Ask the question. Are you interested in how long you live, or how low your cholesterol is? I would contend you want to live longer. If I showed you a study of 12.6 million people, followed for some 10 years and having 694,000 deaths, you would say, "Sounds like a pretty good study to me - it's got big numbers." Well, they found that the ideal cholesterol was between 210 to 249. Sounds like the crack is getting bigger.

Ok, so just what benefit do I get from statins? Let's look at that. A study published in the British Medical Journal looking at 6 primary prevention and 5 secondary prevention studies (all they could find that included mortality and had sufficient scientific rigor) showed a surprising finding. The median survival advantage is just 4-5 days. Not much, considering cost, side-effects, and inconvenience. In fact, perhaps just plain nuts except for in very focused situations, like smokers who have had a heart attack. But folks with negative calcium CTs of their heart being advised to take a statin? That's just plain nuts. (Just look at that study. Folks with score of zero had zero mortality.)

Don't get me wrong. Cardiac disease remains the number one killer in America. It's worthy of being addressed. Just find for me the right tools. I would contend that you want to turn off oxidation and the production of small, dense LDLs. Well, now that's a worthy challenge. Once you understand what's happening, you can shape your own strategy to change it for yourself. We have to dive down into your mitochondria and the membranes of your cells. I can't fit it into this column so it's coming next week. In the meantime, consider cutting out sugar and white flour for the whole week. (Hint: if you measured the volume of your LDLs before and after the week, your LDL volume would have gone up. Your oxidized LDLs would have slipped into "safe" territory and your oxidation count would have gone down.). So next week, we will put the icing on the cake (sorry, wrong image), the olive oil on the avocado, and walk you through how oxidation gets started and how that leads to leaky endothelium in your arteries....and that's what we need to be treating. Stay tuned.

www.What will Work for me. I started my monthly 5-day fast mimicking diet this week. My first-morning fasting glucose after a 13 hour fasting period was 103. Ugh. I have such lousy genes. The Whitehall Study shows that every point over 85 on your fasting glucose results in a 6% increase risk of diabetes. Indeed, my father died of diabetes. The fast-mimicking diet will drop my glucose to the 70s by day 5, which gets me briefly into the safe zone. But insulin resistance and diabetes is all wrapped up in leaky artery endothelium, which is all wrapped up in oxidized, small dense LDLs. I'm intensely interested in this topic. And my physiology represents just about 50% of folks who think they are pretty ok and don't have much trouble, until they do. That's why this is such an important topic. But I'm not convinced a statin will help me. I am going to avoid fructose, sugar, and white flour.

References: BMJ Open, Stat News, Sci Reports, JACC Cardiovascular Imaging, Lancet,

Pop Quiz

1. Statins are an important part of cardiac care and prevention? Answer: Oh, such a loaded question. Yes, for a small number. No, for probably most people, particularly for those with a negative cardiac calcium scoring test.

2. And even if I have risk, how much extra life do I get by taking statins? Answer: 4-5 days. If that comforts you. Make sure you use those 4 days well.

3. My muscle aches and brain fog that I get with statins are worth it, aren't they? Answer: You have to decide

4. What is the level of cholesterol correlated with the longest life-span? Answer: between 210-250. Now, oxidized, small dense LDLs, that’s another story.

5. Did you know that the vast majority of primary care physicians have review of their medical decision-making around statins with economic consequences in their salary for not treating people with cholesterol over 200? Answer: Sad, isn't it? Guess who designed those "quality guidelines"? Yes, statin compensated doctors. The problem: you get caught in the cross-hairs.

The Trouble With Diabetes Isn't the Glucose, It's the Insulin

The Problem with Diabetes Isn't the Sugar, It's the Insulin

We have had an increase of diabetes in America and around the world of unprecedented magnitude. We are increasing at about 10% a year, and our health care system has been helpless to decrease it. Some 60% of people in America are on the path to getting it. What gives?

The clue comes in a unique experiment done almost twenty years ago by Ron Kahn's lab at the Joslin Clinic. The core idea from his experiments was that blood glucose is actually a red herring. It's not the problem. The problem is INSULIN resistance. Blood glucose is just a symptom. Your blood insulin is only partially related to your glucose level. The experiment was to genetically knock out insulin receptors in different tissues in lab mice, and then watch what subsequently happened. Every tissue has insulin receptors. Brain, fat cells, brown fat, muscle, pancreas beta-cells, blood vessels, and kidneys were the tissues they chose. All the mice got sick in one way or another, but only the liver and brain knock-outs got high blood sugar. Only the brain knock-out became obese and developed metabolic syndrome. And to put the final irony, the kidney knockout didn't get high blood glucose but got the kidney disease of diabetes anyways.

WHOA! This has huge implications. The logic is a bit complex but nevertheless compelling. It's not the glucose. It's the insulin that causes the illness.

If you think it through, we see the same effect in humans. Insulin deficient type I diabetics take 20 plus years to get kidney disease. But type II adult-onset diabetics already have the kidney disease before they get the high blood sugar. Why? Because they have had surreptitious insulin resistance for years that was not diagnosed. Their insulin level was over 5 and no one blew the whistle.

Why this dichotomy? Insulin is a two-edged sword. It helps control blood glucose, that's one edge. But it also serves as a proliferative agent. It increases the growth of cells. In the heart and kidney, those cells are the smooth muscle cells in the walls of the arteries, and you get heart attacks and kidney failure as a result. (This has been proven in every intensive insulin program ever done: you reduce blood glucose but raise risk of chronic disease. Bummer.)

What causes insulin resistance? We've known this for 20 years, but it somehow doesn't quite bubble up to the top. Finally, a recent review acknowledges that fructose, half of table sugar, (sucrose is glucose and fructose stuck together) is the real enemy. It drives metabolic syndrome starting with insulin resistance in the liver. Soon thereafter, hypertension shows up too.

Fructose is the enemy. But fructose is in every liquid calorie you drink that is manufactured using high fructose corn syrup. Fructose is in almost every prepared food you eat, every mouthful of ice cream you eat, and on and on. Fruit is some 6% fructose, so even that contributes a little but our body appears to be able to handle the quantity that comes with fruit. But more than two servings of fruit a day and LDLs will go up.  But fructose was never in any food prior to this century.  Real food does not have fructose in it.  Period.

What is so awful about fructose? You can't slow it down. It floods into your liver and demands attention. You have no controls or gates that limit how quickly it gets into your liver. It has to be labeled with a phosphate group from ATP, which exhausts your ATP supply. You get an oversupply of acetyl-CoA in the liver and the liver cell panics and switches to making fatty liver. The fat globules accumulate. And that's the beginning of insulin resistance. Guess how badly Big Food wants you to understand this. Guess how much lobbying money goes into not regulating it?

How do you reverse diabetes? It's not weight loss per see, though that may be extremely helpful. You reverse diabetes by focusing on the insulin resistance and your insulin level. This is where the power of intermittent fasting works. By compressing calories into an 8 hour window, your body has burned up it's glycogen stores in 10-12 hours and you then have at least 4 hours of running on ketones, which means the pressure on your insulin evaporates. The first ketones to go are from your fatty liver. As you reduce fatty liver, your metabolic syndrome fades. Or, once a month fast mimicking. Same thing. But you start by stopping the sugar, high fructose corn syrup in particular.

www.What will Work for me. I've measured my insulin on day 5 of my fast mimicking behavior when I eat 800 calories a day for 5 days: 50% fat and 50% green vegetables. It's been as low as 2. Otherwise, my insulin runs 7-8. I'm tip toeing along the edge of metabolic syndrome. So, I'm close to trouble. For the last month I've started skipping breakfast and eating my first meal at least 10 am. I want to see if I can get my A1c down below 5.6, where it appears to have been permanently parked. And no sugar, no sugar, no sugar.

References: Ann Rev Physiology, Critical Rev Clin Lab Sci, Nutrition and Metab, Penn Med News,

Pop Quiz

1. Through most of human history, when did we get sugar? Answer: Only in the fall when fruit ripened which we could get for a couple of weeks. Or, if we found a beehive. Sugar has shown up in our food supply only in the last 100 years in quantity.

2. And just what does sugar (fructose in particular) do to make metabolic syndrome? Answer: Insulin resistance.

3. Which comes first for adult-onset diabetics, the high blood glucose or high insulin? Answer: Insulin is way first. If you had observed the range of "normal insulin" in our labs in Southeast Wisconsin over the last 30 years, you would have noted that the "range of normal" has been creeping up every couple of years. The supposed normal range is now typically 3-29, depending which lab you use. It used to be 1.9-19 about 15 years ago. What happened in the interim? We have eaten more HFCS, ice cream, sugared sodas, ketchup....etc.

4. What is the cardinal first step in lowering your insulin? Answer: It starts in your fatty liver begging you to stop the fructose. Then, give your liver a break and let it burn up all the energy you stuffed into it with fructose by lengthening the time you don't eat each day. Get to 16 hours, your fatty liver will go away.

5. What is a healthy insulin level? Answer: Less than 5. Measure it. Pay heed if it's higher.

6. Can you take enough meds for diabetes to reverse the harm of fructose? Answer: No. Meds are just a bandaid to cover the symptom of high blood sugar. High blood glucose is the symptom. High insulin is the disease.

Plasmalogens and Parkinson's disease

Plasmalogens and Parkinson's Disease

Parkinson's is the number two horrible neurological disease plaguing the elderly and has been increasing as the population ages. It is classically known as a loss of dopamine-producing cells in the substantia nigra, a tiny little nucleus at the base of the brain. Its symptoms include a mask-like face, rigid walking and movements, a pill-rolling tremor, and eventually cognitive decline. It's miserable.

Giving dopamine back as a medication, or stimulating more release of dopamine helps for a while, but the real problem is the inexorable depletion of those precious few remaining cells in the substantia nigra.

In the 1980s, a couple of California folks were trying to make designer heroine. They stumbled onto a drug called MPTP, which unfortunately gave them Parkinson's in a real fast sort of way. The drug, MPTP, turned out to be a perfect model for creating Parkinson's in lab animals. Over the years researchers have been able to drill down to the exact chemical steps that happen. The MPTP is a poison to your mitochondria all over your body. But it is preferentially taken up by dopamine neurons, so they get a super boost of it, and it kills their mitochondria off. The dopamine-producing cells die and the lab mice get Parkinson's in a dose-dependent fashion. But wait, there's more. It turns out the MPTP has been a perfect study drug to elucidate the electron transport chain, which MPTP poisons in Complex A. That's where you are meant to turn NADPH (a source of free radicals) to NAD+, safe. With MPTP around, NADPH backs up and you make boatloads of free oxygen species, which your cells desperately try to get rid of by making peroxide. (If you want to be a biochemistry snob, you can quote that the NOX enzyme on the surface of your cell is what captures that extra NADHP and spits out the peroxide outside the cell.) Peroxide in your blood activates glia cells and those activated glia turn into cookie monsters and gobble up the injured cells.

Ok, what's the big deal? The big deal is that is the precise mechanism for cell death in the brain from all causes that make too many reactive oxygen species for all sorts of reasons, and which is fixed by having more plasmalogens. Like Alzheimer's. Like ALS. What did I just say? Fixed by more plasmalogens. Plasmalogens are the membrane lipids with a "vinyl ether bond" that gobbles up peroxide and neutralizes it. It is the backup protection for overloads of reactive oxygen species. It is the reservoir of protection that allows you to have a short-term bump in reactive oxygen species, and recover. And when you run out of that reserve pool, you are more vulnerable to getting Alzheimer's and ALS if you don't get Parkinson's.

So, just what do we know about plasmalogen blood levels in folks with Parkinson's? From Dr. Goodenowe's study at Rush in Chicago, we know that blood plasmalogen levels are incredibly predictive. Healthy blood levels and Parkinson's is a rare disease. Low levels and risk skyrockets. Everyone with Parkinson's has lower levels. Very similar to Alzheimer's and ALS.

Ok, what are the plasmalogen's doing? Well, Goodenowe has now completed multiple lab mice studies of MPTP. If you give extra doses of Plasmalogens to the mice before they get exposed to MPTP, they never get the expected Parkinson's. If you give the MPTP and wait 5 days, they still don't get it, or at least much less.

Alright, one final study. Let's take monkeys that have been given MPTP and had Parkinson's induced. They are now down the road with bona fide Parkinson's, on L-dopa, and being successfully treated. Just like with humans they are beginning to get the typical dyskinesias of long-term L-dopa therapy. Give the monkey's plasmalogen replacement therapy and guess what happens? Some 30-50% reduction in the dyskinesias. This means the plasmalogens are acting beyond just being protective by sucking up peroxide. They are making the remaining neurons function better because they play a role in the synaptic membrane of helping the packets of dopamine to be released faster and better. That's a neuroactive function in itself.

Where are we in human Plasmalogen research? It's just emerging. A study from Japan showed improvement in Parkinson's symptoms when given oral plasmalogens derived from scallops. Their dose was 1 mg a day, which is hard to reconcile, being such a low dose.

But everything is lined up. First and most important, plasmalogens are fats that are just food. They are not toxic in any way. You just have to get a form of them that gets into the body. The normal, animal-based plasmalogens, are digested in your stomach. Almost 100%. Goodenowe has invented a product that delivers a bio-active template that gets into your body, allowing you to make the right stuff.

www.What will Work for me. Again, we are seeing how plasmalogens play roles in the core functions of our neurological systems. The point is not to treat the disease necessarily, but to catch people as soon as they might be at risk and normalize levels so that they aren't prone to the subsequent risk. I now know that plasmalogens play many, unique and critical roles: they are your body's main depository for omega-3 fatty acids, they help your hormonal vesicles merge rapidly by shape-changing, they neutralize hydrogen peroxide and finally, they are the most liquid of membranes, allowing proteins embedded within them to move rapidly and smoothly. Pretty impressive. We are down to the very core of how our bodies work. This is "membrane science", a new and critical field of inquiry that undergirds just about every aspect of our medical spectrum. Interesting.

References: Parkinson's Disease, Br J Pharm, Behavioral Brain Research, Jr of Neuroinflammation, Free Rad Biol Med, Free Rad Biol Med, Aging Research Reviews,

Pop Quiz

1. If I have low blood plasmalogens, what happens to my risk for Parkinson's? Answer: Much higher.

2. If I have Parkinson's, what happens when I raise my plasmalogens with supplements? Answer: Early results show improvement

3. What is happening in my brain cells if I take Plasmalogens? Answer: they are the lipids that can shape change, a critical feature for membrane fusion: a fancy term for what it takes to put neurotransmitters into the synaptic junction.

4. Why do my plasmalogens get low? Answer: Likely an environment of elevated oxidizing compounds. Some folks must be more vulnerable. Research pending.

5. Is there any risk to taking plasmalogen supplements? Answer: Nope. No more risk than eating a teaspoon of olive oil. It's food.

Plasmalogens and Cancer

Fight Bowel Cancers and Inflammatory Bowel Disease with mRNA-148 and Curcumin

Ok, the title is a mouthful. But the story is amazing. If you understand this, you may conclude that we are at the threshold of detecting bowel cancers much much sooner, and more importantly preventing/treating it more effectively. So this is big. Having had several family members diet of colorectal cancer, I've got skin in this game. (And very likely, ALL cancers.....)

The first concept to understand is that your gut makes very, very-long-chain fatty acids (GTAs-gastrointestinal tract acids). Not the run of the mill 18 carbon-long fatty acids stored in your fat cell, I'm talking 28-36 carbons long. Super long. And they are strongly anti-inflammatory and very cancer-protective. If you have tons of them, you are a lucky devil. Your risk of GI cancers is very low. And they are low years before colon cancer develops. That makes them very effective screening tools. If you are low, you are at a much higher risk of getting colon cancer. Curiously, carving out the cancer with surgery doesn't lower their level. Their low level PRECEDEs the cancer. You want a higher level, or else a second cancer has fertile soil to grow in.

What are these GTA's doing? Well, for one, they are incredibly potent anti-inflammatory compounds. If you look at the activity of folks without GTAs in their blood, their NFkappaB is much higher. There are about a dozen markers of inflammation that are downregulated. You may have heard about LPS caused inflammation? Yes? LPs are the lipopolysaccharides off the walls of bacteria that get into your blood and set off inflammation. Guess what GTAs do? Yup - cut them off completely. Cool, huh!

Want to get better? You've heard about how curcumin cuts off LPs inflammation? (Say yes and pretend you have.). Well, it does. Particularly in the brain. We have known that South Asians who eat curcumin breakfast, lunch, and dinner have much less Alzheimer's and many fewer cancers than Americans until they leave South Asia and adopt diets without the curcumin. Now, not all curcuminoids are equal. Of the three known curcuminoids, I and II have very little effect but III, which has two "methoxy" groups carved off is the real deal. It turns on miRNA148 like crazy. And that's the secret sauce that fights cancer, inflammation, and inflammatory bowel disease. The problem is is that it is only 1-1.5% of curcumin. You want MORE. Micro RNAs are short messenger RNA that are only some 22 bases long. They act like genetic switches turning on and off different genes. Learning how to manipulate them is the next huge frontier ahead of us in medicine. And miR-148a appears to be a champion cancer killer. You want it on your side with colon cancer, pancreatic cancer. Like the GTAs, miRNA-148 is low as an inherent part of the cancer. It's like the cancer can't behave like a cancer without first suppressing mi-RNA-148. Then, when it's suppressed it can migrate and spread and be wicked.

Now, let's talk colitis and inflammatory bowel disease. The inevitable and dreaded consequence of that is colon cancer. Guess what happens to mice with the lab model of colitis who get their miRNA-148a stimulated? You got it. Cancer is stopped almost completely back to normal healthy mice. Read that again! Click the link. Guess what stimulates miRNA-148a? Turmeric, particularly the type III (the 1% stuff.)

Now, round out the portfolio of risks for colon and pancreatic cancer and Goodenowe has found the inevitable. Lower production of healthy plasmalogens by choline-deficient diets with more inflammatory arachidonic acid instead of DHA caused by too much omega 6 fatty dietary fats (fried food with vegetable oils), and you shift the whole membrane biology towards more cancer. You can reverse that too by making sure you have sufficient choline in your diet and less O-6 fats.

www.What will Work for me. Put this all together and we are talking a strategy that will reduce your risk of cancer may be on the order of 10 fold total. No kidding. I have low GTAs in my blood. That means I am at higher risk for colon cancer. I will be taking that turmeric-3 product for the rest of my life. Goodenowe has gone on to manufacture the Type III Tumeric molecule under the name Prodrome GTA. You can't buy it directly but if you are an active client, just use my name and we will back you up when they call. You will get a discount. When I go over the results of Goodenowe's metabolic scan of various clients, he has repeatedly pointed out various profiles that are at high risk of ovarian, colon, pancreatic cancer. Doesn't mean those folks have it, but it is something that can be reversed, and dramatically proven by the published science. This will be the future of cancer prevention: detect the biochemical phenotype earlier in life and in those with abnormal findings, much more frequent screening tests, or better yet, more aggressive supplementation with neutralizing dietary compounds.

Summary of better diet: turmeric as often as you can eat it. Less vegetable oil and more fish oil. More choline. (Eggs, chickpeas...)

References: BMC Gastroenterol, BMC Medicine, International Jr of Cancer, J Ex Clin Can Res, Oxidative Med and Cellular Longevity, Frontiers in Pharmacol, Progress in Preventative Medicine, BMC Genomics, Human Cell, Onco Letters, Exp Ther Med,

Pop Quiz

1. Just what are GTAs? Answer: Super long-chain fatty acids made in your gut. They are anti-inflammatory and anti-cancer compounds.

2. What can you do to make more of them? Answer: We don't know right now.

3. What can reverse their absence? Answer: Turmeric, specifically Type-3 with the two methoxy groups off it.

4. Can I alter my profile? Answer: Yes. Eat like a South Asian. Lots of curry, every chance your get. If you want to push the envelope, buy Prodrome GTA which is 50% bisdemethoxycurcumin)from the Prodrome company. Cut down your fried food. Eat more fish and chickpeas and eggs. (Or take alpha-GPC)

5. If I have a cancer, can I suppress it with turmeric? Answer. Yes, 1% with the normal stuff. I would personally be all over the Prodrome GTA and Prodrome Neuro supplements. They are precision food for naturally fighting cancer.

Plasmalogen Loss Drives Coronary Artery Disease

Plasmalogen Loss Drives Coronary Artery Disease

At last, we are down to the basic, basic biology and understanding of how coronary artery works! Dr. Dayan Goodenowe in his discovery and development of plasmalogens in human disease has opened a door of understanding that finally is creating a construct we can wrap our brains around and bring understanding to the very core of human illness. This is like the Unified Theory of particle physics. It's all about the balance of your "redox" capacity and health down at the molecular level. Let me see if I can explain it in understandable language and how that relates to your arteries in your heart.

You first have to start with the "endothelium" of your arteries. That is the inner cell layer surrounding every artery. It is pretty stupid. It only has three jobs. One: constrict or squeeze in. (We call that high blood pressure or endothelial dysfunction). Two: it relaxes. (This is normal blood pressure and that's good - healthy, optimal.). Three: it can call for help. It has millions of TLR's (tiny little radars) that are constantly monitoring to see if you have been invaded by germs. Ok, and all of that depends on the endothelium being intact. By intact, I mean all the cells are tightly connected to each other. The very first step in coronary artery disease is the advent of "leaky endothelium". That is caused by hydrogen peroxide being released from a variety of sources. There is good proof on this account in that we can see the damaging effect of homocysteine being broken down to uric acid and making peroxide on the way. And blood tests of higher uric acid and higher homocysteine both correlate, sure enough, with more artery disease.


Well, what happens when you get that leaky endothelium? Ah! That's when oxidized LDLs can wiggle their way into the wall of the arteries. That starts the accumulation of more LDLs and the generation of foam cells. Eventually, that plaque builds up and plugs arteries up, causing a heart attack, or the plaque ruptures and gunk flows downstream and causes trouble there. This is how strokes get started.

How do we know plasmalogens are involved? Multiple studies from a variety of sources have demonstrated this effect. A very elegant publication on dialysis patients showed that those who died from heart disease had much lower plasmalogens than those who didn't. Plasmalogen levels are a pretty good indicator of "oxidative stress" and low levels are dangerous.  Low plasmalogens, you get a heart attack!  High plasmalogens, you don't.  Simple. That's one.

Another great study was in Atherosclerosis in 2017. In that study, they showed that folks with peripheral vascular disease have very high risk of heart attacks in the next few months, and that risk is proportionate to how low their plasmalogen levels are. Doing an angioplasty on or bypass surgery on your narrowed arteries doesn't fix the "endothelial dysfunction". Repairing your plasmalogens does! This is huge!

We can go on! Another study from another angle, also in the journal, Atherosclerosis from 2015, looked at HDLs, high-density lipoproteins. They are meant to be protective against heart attacks. They exert their effect partially by protecting those precious "endothelial cells" lining your arteries from dying through the process called apoptosis. With low plasmalogens, they don't protect them from apoptosis.

You can have an angioplasty of every artery in your body but you haven't reversed the disease, you have only repaired the short-term symptom.  Come back in 6 months for a second angioplasty.  Fix the plasmalogens and you have gotten to the core disease process.  Then, you don't come back.  Fixing blocked arteries is big business and big bucks, and doesn't really work. Fixing plasmalogens is cheap compared to one angioplasty, and it works.

The basic disease is the loss of plasmalogen "redox" capacity, the ability to soak up and neutralize reactive oxygen species by that precious vinyl-ether bond built into the plasmalogen. What causes the depletion of plasmalogens? Ah, there is the mystery of modern civilization.  In biochemical terms, it's loading too much NADPH into the mitochondria and leaking out too many reactive oxygen species.  In lay terms that we understand it means too many calories, too much sugar, too little exercise, too many environmental toxins, too little sleep, not enough exercise......If you want to go down that rabbit hole, read Biochem Biophys Acta article on Aging Peroxisomes and how they make less catalase. Less catalase means more hydrogen peroxide floating around in your blood. What does that do? If you get that right, I've succeeded in introducing you to this topic. ............(Did you get it?) Catalase breaks up hydrogen peroxide and thereby protects the lining of your arteries from getting leaky. What do plasmalogens do? They are the fatty acid molecules in every membrane that have the ability to soak up damaging "oxidants". But they get used up when can't make them as fast as we use them up.

www.What will Work for me. I'm getting older which means like it or not, my peroxisomes are not as robust as they used to be. I'm walking every day. I'm doing intermittent fasting and avoiding sugar as best I can. But darn it, this last week I had a birthday and I had a little cake. Life happens. But I am taking Dr. Goodenowe's Plasmalogen replacement supplements every day. My bet is that this keeps me away from the cardiologist's angioplasty suite. Fish oil is one of the key building blocks of these precious plasmalogens. That's why you want sufficient fish oil in your diet. But old peroxisomes, where plasmalogens are made, remain old and less functional. You can't un-age them, yet. You can take plasmalogen replacement therapy.  That should be a slam dunk.

References: Nephrol Dial Trans, Atherosclerosis 2017, Atherosclerosis 2015, Biochem Biophys Acta, Biochemical J,

Pop Quiz

1. What is "endothelial dysfunction"?                     Answer: The first step towards artery disease with fatty lipids being deposited as the end marker. You get a leaky endothelium with the subsequent ability of oxidized LDL's to seep in.

2. What is the root cause of it?                           Answer: Too much hydrogen peroxide in your arteries, caused by insufficient catalase to neutralize it.

3. Where does catalase come from?                         Answer: It is an enzyme made in your peroxisomes. Your peroxisomes are in every cell of your body, right next to your mitochondria. Their job is to make plasmalogens and catalase, and feed mitochondria their basic, preferred fuel of fatty acids.

4. What's the best way to fix the disease called "heart attack or stroke"?                     Answer: If you are having those, the best treatment is to immediately go to a hospital and repair the damage that's happening ASAP. But that is just symptom repair. The long-term cure is to fix your plasmalogens.

5. Is this the end of coronary artery disease?                   Answer: Are you kidding? The power of the sugar lobby, the couch potato lobby, the trans fat, the pesticide, the toxin, the .......

Feeling Tired All The Time: Blame Ceramides

Energy a Bit Low? Blame Ceramides

Do you feel washed out and tired after a meal, or at the end of the day? Dragging around, wishing you had a pick-me-up to get some get-up-and-go? Is your energy level curiously just rotten? Read this.

We are beginning to get a better understanding of how our energy flow works through understanding core metabolic processes right down in our mitochondria, our local energy factories. (Remember, you are 10% mitochondria! Your heart and brain are closer to 30%.). Mitochondria make energy in the form of the molecule ATP. So far, so good. But here are some guiding principles in making energy I bet you weren't aware of. Did you know that your mitochondria are really happiest if they can switch back and forth between running on fat or running on glucose? Did you know that they do better when you are on just one pure source of energy (glucose - carbs) or fat ( beta-hydroxybutyrate.) and not mixed. When you mix sources of fuel, it's like having two hoses filling your gas tank on your car. Something overflows. You get more reactive oxygen species (ROS) and that makes for more damage? Did you know that you start to drift into ketosis if you don't eat for 12 hours? Yup, and more ketones at 14 and even more at 16. But too much of fat, carbs, protein all at once, a typical American big meal, and your mitochondria get overwhelmed with too much fuel. And some of if is just plain bad.

Bad fuel #1 is fructose. Now, through most of human history, we got ripe fruit (hence fructose at about 5-6% of ripe fruit) only in September for a few weeks. Or, for any of us with a mulberry tree in their yards, you can imagine snarfing down mulberries all day long for about a week in July. We only got sugar, half glucose, and half fructose, in about the year 1500 or so, and only ramped up to 120 pounds a year each in the last 40 years with the addition of high fructose corn syrup. Fructose at such quantities is a new phenomenon to our mitochondria. The problem with fructose is that we don't have a way to slow it down. It goes straight to your liver, kabam! Your liver cannot turn it away. We exhaust our liver cells that frantically try to protect themselves by making fat and scavenging ADP into AMP and then uric acid. If you have fatty liver or high uric acid, you are probably well-served if you seriously examine your sugar intake because you are tip-toeing along the edge of liver failure. If you don't believe this, watch the movie "Super Size Me" and see someone who almost died from eating at MacDonald's three times a day for a month.

We now know how your liver cells protect themselves. They make ceramide fats and palmitic acid (16 carbons long) from all that fructose. Ceramides are stiffer molecules than most fats, making your cell walls more rigid and less capable to taking up arriving nutrients. Ha! Short-term strategy works. It saves the cells. But another, more insidious event happens. Ceramides block the insulin receptor, in part because of their stiffening effect on the cell membrane. And that, my friend, is how insulin resistance gets started. Your rising level of insulin corroborates with inflammation, and you now have adult-onset diabetes off to the races. With high levels of insulin in your blood, your fat cells get the message not to open up and share their fat. You have the perfect double whammy to blocked glucose uptake (so less energy) and locked fat cells (less energy).

You are in a dilemma. You have plenty of stored energy. Just check out your fat tissue. But you can't get to it. And the only, only way to feel good is to eat enough glucose to get huge swings in blood sugar and then plunges thereafter. See-saw, see-saw. And you are exhausted to boot.

Once you understand the mechanisms, you can find the way how to climb down off this cliff and get your mitochondria back to working. You can measure your ceramides if you are curious. You can certainly measure your A1c to see how "diabetic" you are. You can measure your insulin level. It should be below 7 at the worst. Five would be better.

Key principles to fixing yourself is stopping the fructose and slowing way down processed carbs. Then, focus on rebuilding your mitochondria's ability to be metabolically flexible by stretching out the time between meals, particularly at night. That way you burn up all your carbs and get practice at switching over to fat. Add more green vegetables that also make beta-hydroxybutyrate and you ease away from glucose carbs. Add olive oil. Reduce your protein down too. And all those together will get you back to metabolically flexible, with more energy and fewer ceramides. You can do it.

Did you know that ceramides predict your risk of heart disease more accurately than LDL cholesterol? Yup...but that's for another day.

www.What will Work for me. How to lower ceramides? Well, well....that's the question. Start with cutting the sugar out of your diet. If you wanted to really cut the sugar, that means you have to take on ketchup and peanut butter too! Eating extra olive oil in a Mediterranean diet has been shown to reduce heart disease commensurate with its ability to lower ceramide blood levels. More green vegetables in your diet delivers more beta-hydroxybutyrate to your mitochondria, slowly. Intermittent fasting, compressing your calories into 8 hours does it too. Hmm. I'm fasting for 5 days a month. Perhaps I need to learn to navigate past breakfast too. I found a ceramide blood test on Goodenowe's plasmalogen test. Mine was higher than I like. Bummer.

References: JAHA, Nutr Met CV Dis., Nature Metabolism, FASEB, American Coll Cardiology, Mol Nutr Food Res. , Circulation, Biochem Biophy Acta,

Pop Quiz

1. What are ceramides? Answer: they are a rigid fat that makes membranes firmer, or stiffer. (Not good)

2. What is the key means by which you make them? Answer: Eating fructose in the form of too much HFCS, table sugar, hidden sugar, fake names for sugar (like dehydrated orange juice), and forcing your liver to make palmitate, which then hits your mitochondria hard.

3. What would your mitochondria prefer? Answer: Mitochondria want to get back to metabolic resiliency and the ability to flex between carbs and fat. You can do that by compressing calories into 8 hours a day. You naturally do it when you exercise to exhaustion. You get there faster if you eat more vegetables and more olive oil.

4. If your mitochondria get overwhelmed and your cell responds by making ceramides, what happens to your ability to make ATP energy? Answer: It goes down. So do you.

5. Can I measure ceramides? Answer: Just emerging. Not yet in the major labs and certainly not in your regular clinic. The Mayo Clinic is all hot on it and has it. Goodenowe measures them with his blood panel. (