Is shock therapy the answer to “cure” obesity?

10. August 2014 Lisa G (0)
The next obesity “fix” may be hitting the market known as "VBLOC therapy”.  This implanted device delivers intermittent electrical "blocking signals" to the intra-abdominal vagus nerve.  According to the manufacturer, the device "reduces sensations of hunger and produces satiety leading to weight loss.”

Seems to me like another classic case of conventional healthcare proposing surgery or medications to address the obesity epidemic. Pharmacologic treatment and bariatric surgery have been offered for years to win the battle of the bulge.  As a registered dietitian, who years ago begrudgingly counseled patients prior to undergoing bariatric surgery, I have seen countless people re-gaining all (if not more) of the weight lost after the first year of surgery. Same goes for pharmalogical interventions, such as Phentermine.  Sure it worked in the short-term.  But in every single case, when the medication was stopped, as it is not FDA approved for long-term use, the weight came creeping back.

My take on the releasing a significant amount of weight does not require going under the knife.  How about this instead? Address the cause of increase hunger and appetite.  This is a crucial missing link for many undergoing surgery or using medication(s) as a “solution”.  Not addressing the cause of increased hunger and ravenous eating behaviors precipitously results in rebound weight gain.  Rather than sending an electrical pulse to a nerve in the stomach, maybe the FDA should consider a Cureality-based nutrition program that is wildly successful stimulating a “side effect” of weight loss.  Wheat elimination offers a surgery-free option that reduces hunger and insistent drive to eat every few hours, thanks to freedom from gliadin driven appetite stimulation.  Weight loss is common experience due to reduced hunger and subsequent intake. Give it a try.  What else do you have to lose, but some love handles?

--Lisa Grudzielanek, MS,RDN,CD CDE
Cureality Nutrition & Health Coach

Are Your Beauty Products Toxic?

10. August 2014 Lisa G (0)
As a nutritionist and self-care advocate, I am very careful about what I put in my body.  Health benefits experienced through proper nutrition are well understood.  We avoid highly processed foods, wheat-based products, and sugary snacks because we know that are “unhealthy” for us.  But what about what we put on our skin?

An important piece of the health and wellness puzzle is not only what is on the end of our fork but on our toothbrush, slapped on our bodies and rubbed into our hair.  Skin is the largest organ and what we place on it on a daily basis penetrates the skin, enters the fat stores and contributes to the toxicity and adiposity of our bodies.  According to the Environmental Working Group, the average woman uses 12 beauty products per day, containing about 168 ingredients.  Yikes!

I’ve often held a high suspicious that endocrine disruptors such as parabens, triclosan, fragrance, and other punitive chemicals are a key suspect in the root cause of my endocrine disruption.  Interestingly, scientific evidence is now emerging to support this suspicion.

A few months back, I took a look at my hair, skin, and cosmetic products. I was shocked and horrified.  Parabens, an estrogen-mimicking preservative linked with endocrine disruption, was in dozens of products.  It reminded me of how I felt on that day years ago when I threw out all the products in my kitchen that contained wheat.  What are parabens not in?  Why was it in so many products?

In our next episode of Cureality Connections we will discuss key skin and beauty product chemicals to avoid along with other steps to take to attain beauty from within.

--Lisa Grudzielanek MS, RDN, CD, CDE

Top 3 Strength Training Exercises for Runners

28. July 2014 Amber B (0)
First and foremost, if you’re a runner and you’re not strength training you need to start.  This in and of itself could be an entire blog article.  But here I go with the synopsis. 

Strength training will indirectly help you run longer and faster.  Strength training exercises can improve your running mechanics, so that you run more efficiently.  Efficient running mechanics will lead to less wasted energy with each step and less injuries. 

Think about it.  You will take 80 to 90 steps per foot each minute you run.  If you have muscular imbalances that lead to joint mobility or stability issues you will move through an improper range of motion with each step. 

When you run for 30 minutes you take 2700 steps with each foot for a combined 5400 steps.  That could be 5400 steps of feet rolling in, rounded shoulders, wasted side to side movement or just pure pain.  Needless to say, when you are an endurance athlete it’s important that each step and every workout is adding to improved performance not to injury or fatigue.

The key to becoming a better runner is consistency.  For most runners, injuries are the biggest disrupter of consistent training.  Runners get a few good weeks or months of training, and then they are injured.   That means time off, loss of motivation, and a decrease in fitness. 

Strength training with proper form 2 to 3 times a week will reduce the onset of injuries and improve your running form.  Here are my top 3 strength training exercises for runners. 

Bulgarian Split Squat

You will need a bench, chair or stepper to perform this exercise.  Start by doing this exercise with just body weight and then progress.  The progression could include holding dumbbells, kettlebells or a barbell.  You can also make this exercise explosive. 




 
  • Place the to top of your back foot on.  If you are having a hard time with balance, flex your back toes and place them on the bench.   
  • Stand in a staggered stance about 2 to 3 feet wide.  This should allow your knee to bend while keeping your knees behind your front toes. 
  • Inhale as you begin to bend both knees. 
  • Focus on your back knee pointing straight down toward the ground and your body weight in your front heel.   
  • Keep your front kneecap inline with the 3rd toe of the front foot. 
  • Exhale as you straighten both knees to come back up to standing.  
Start with 10 repetitions on each leg and progress to 15. 

Calf Lowers

Use a stair or a stepper to perform this exercise.  Start by doing this exercise with just body weight.  The progression would include holding a dumbbell in one hand. 


 


  • Place the ball of your foot on the stair while holding on to the wall or railing.   
  • Rise up on the ball of your foot as high as your heel will go.  Make sure you have weight evenly distributed on all of your toes and that you are not rolling onto one side of your foot. 
  • Slowly, lower you heel back to the starting position.  Try counting 3 to 5 slow counts to ensure you really focus on lowering part of the movement.   
Do 10 reputations on each foot to start.  Work up to doing 20 reputations on each foot. 

Band or Cable Row

How many runners do you see hunched over logging long miles.  This exercise is for improved running posture, which can lead to improved respiration. 

To perform this exercise, use a band or a cable.  This exercise can be done with both arms or with just one arm. 





  • Stand in a staggered stance with relaxed knees.  Make sure your ribs on stacked on top of your hips to ensure good posture. 
  • Grab the handles of the band or the cable in the thumbs up position. 
  • Start the movement by protracting the shoulder blades.
  • Then bend the elbows straight back so that your biceps are close to your rib care.  Keep  your knuckles forward. 
  • To release, begin to straighten your elbows and bring your shoulders back to the starting position. 
Start with 10 repitions and work up to 20.  To increase difficulty, use a more difficult band or more weight on the cable system. 

Here’s to improving your running mechanics so that you can train more consistently.  Can’t wait to hear about the PR at your next race. 

How did Cureality get its start?

27. July 2014 William Davis (0)



In the Cureality program, we embrace information and strategies that empower you in health without drugs, without hospitals, without procedures. We convert your doctor from director of healthcare to your assistant in health. He or she is there when you need help, but you largely direct your own health future.

How did we gain the know-how, information, tools, even chutzpah to take on such an ambitious project?

It started around 10 years ago with the awkwardly named Track Your Plaque program. In fact, some of the current followers of the Cureality program are former Track Your Plaque members, having learned of the wonderful list of strategies that can be adopted to gain better control over, even reverse, coronary atherosclerotic plaque and risk for heart attack. They also learned that something special happens when you engage with other people with similar interests, all sharing ideas, insights, and resources to get the self-directed health job done. Over time, what started out as simply a source of better information for coronary health evolved into a self-directed coronary disease management program. We never set out to create something as wildly ambitious as a do-it-yourself-at-home coronary disease risk management program, but that is how it inadvertently turned out.

How we went from Information Provider to Health Empowerment Program

So we never intended to take on something so seemingly impossible as managing coronary risk on your own. But, because we armed people with such empowering, profound insights into better ways to manage their heart disease risk beyond “don’t smoke, cut saturated fat, be active, and take a statin drug”—the typical advice offered by doctors—they returned after an interaction with their doctors disappointed: doctors often declared such strategies unnecessary, or the doctor didn’t understand them—even when there were clear-cut clinical data already available to support their use. In other words, the patients—everyday people, not experts—knew more than their doctors. 

This flip-flop in the balance of knowledge made for some very interesting stories, like “Harold” (not his real name) who, having survived a heart attack and received a stent, was told by his doctor to cut his fat intake, eat more whole grains, exercise, take aspirin and a beta blocker drug, and reduce his cholesterol values with a statin drug. Upon learning all the additional information from the Track Your Plaque program, Harold returned to his doctor and asked “I’m not so ready to just go along with this idea of ‘reducing cholesterol’ to address heart disease risk. Because my goal is to gain as much control over coronary disease as possible, maybe even reverse it, I’d like to address some additional issues that I believe may be important. I’d like to have my advanced lipoproteins drawn to measure the proportion of small LDL particles I have, whether I have lipoprotein(a), an omega-3 fatty acid index and 25-hydroxy vitamin D level, and a thyroid assessment. Oh, and I believe I should also have an assessment of my inflammation status, perhaps a c-reactive protein and phospholipase A2, and my blood sugar status measured with a fasting glucose, insulin, and hemoglobin A1c.” Harold’s doctor was dumbfounded and speechless. Rather than reveal his ignorance, his doctor advised Harold that none of that was necessary, sending him on his way and telling him that he was fine.

But this left Harold with a sour taste in his mouth, having engaged in many online discussions with people who had followed conventional advice that resulted in more heart attack, more heart procedures—the conventional answers simply did not work. He also discussed his situation with people who had successfully obtained the additional information he sought, added it to their program and enjoyed dramatically improved health, including freedom from more heart attacks, heart symptoms, and heart procedures, as well as improved overall health. So Harold found an easy way to obtain the testing on his own. Within a couple of weeks, he returned to his online community and shared all his information. Within moments, he was provided useful discussion to help him understand the values, all leading to changes in nutrition, nutritional supplement choices, how and where to get the simple tools necessary, such as iodine and vitamin D supplements. He even entered his data, choosing which values he was willing to share with others, which remained private, allowing him to compare his own follow-up values several months later. Engaged in this process, self-directed but collaborative, he witnessed marked transformations in his health. Not only did he never again—over several years—ever re-develop heart symptoms nor require any more trips back to the cath lab, he lost weight, reversed a pre-diabetic sugar profile, improved his cholesterol values without drugs, got rid of the acid reflux symptoms he endured for many years, dropped his blood pressure to normal, enjoyed better mood, energy, and sleep. Slender, healthier, all accomplished without his doctor. 

Harold returned to his doctor for a routine follow-up. Slender, energetic, without complaints, on no drugs except the aspirin for his stent, the basic laboratory assessment his doctor ordered in front of him, his doctor admitted,” Well, I don’t know how you’re doing it, but these values look like a 20-year old substituted his blood for yours. They’re unbelievable. What drugs are you taking to do this?” “No drugs,” Harold replied, “I’m following a program to reverse heart disease, but it means doing some things that are different from conventional solutions.” His doctor closed their meeting with the signature response of doctors nationwide: “Well, I don’t understand what you are doing, but just keep doing it.”

Yes, Harold knew more about how to control heart disease than his doctor, more than his cardiologist. The cardiologist knew how to insert a stent or defibrillator. But deliver information that empowered Harold in all aspects of health from head to toe, while also dramatically reducing, perhaps eliminating, his coronary disease risk? As you now know, that is not what conventional healthcare does, nor is it interested in doing so, as it would relinquish control and threaten to cut off this hugely profitable revenue stream that drives “healthcare.”

Having managed to inadvertently create a self-directed coronary risk management program with such spectacular results and in probably one of the most difficult areas of all—heart disease—it became clear that a similar approach could be even more easily applied to many other areas of health, such as weight loss, bone health, cholesterol and blood pressure issues, diabetes and pre-diabetes, hormonal health, autoimmune conditions, and others. You can do it when empowered by safe, effective information, and supported by a community of sharing and collaboration. We don’t fire our doctors; they are there when we need them when, for instance, we get injured or catch pneumonia, or as an occasional resource. But doctors should no longer be able to get away with neglect, misinformation, or blindly directing you to the next revenue-generating procedure because you are empowered by the information and support you receive in Cureality.

As we get more effective in delivering this information and new tools to you, just imagine what we can accomplish in this new age of information and self-empowerment. The future for us is bright with ambitions for better interactive tools with Cureality expert staff, better ways to crowd source health answers, provide more engaging community conversation, all while the health insights that help accomplish our self-directed health goals get better and better. Each person that joins Cureality helps make this service more effective because your wisdom, insights, and experience are added to the collective knowledge. We are more powerful together than we are as individuals.

If you are already a Cureality Member, please add your comments and questions to the growing conversation. If you are not a Member, consider joining our discussions, as each new voice gets us closer and closer to better answers to take back control over health.

Sit Less and Move More.

21. July 2014 Amber B (0)


We sit way too much. Many of us have desk jobs where we sit for 8 to 9 hours a day. After we leave the office, we sit in our car to run errands. We follow that by sitting down to eat dinner. Our day ends by sitting on the couch to unwind by watching some television.

Many of us will be sitting a good 12 to 15 hours each and every day. Unfortunately the research shows that long hours of sitting can lead to obesity, heart disease, diabetes, and even early death. Don’t be fooled that your workout is enough movement. You can still be active and sedentary.

How can you add more movement to your day? First, think about all the times you find yourself sitting during the day. Then come up with a creative way that you can get out of the seat and move your feet.

Here are a couple of examples:

Instead of driving everywhere, jump on your bike. The picture above is of the bike I use to go to work or run errands. Bike riding is great exercise, greener transportation and a great stress relief.

We spend a lot of time at work sitting in front of the computer or the phone. Prop your laptop on a bookshelf to create a standing workstation. You can also purchase a sit-stand workstation you can adjust throughout the day. Get a headset and stand during phone calls.

Walk during your lunch break. Walk to the coffee shop, the mailbox, and the dry cleaners. Get your errands done on foot or just enjoy a stroll outside.

Take a movement break every hour. Do some desk push-ups, squats or walk the stairs. Need to communicate with a coworker? Don't email, walk over and talk to them.

Human beings are meant to move, not sit in chairs all day. I want to challenge you to incorporate more movement into your day. I'd love to read your comments how you move more and sit less.

Have You Had Your Prebiotics Today?

11. July 2014 Lisa G (0)


Prebiotics and resistant starch may be the missing link to your digestive health. Indigestible fibers that allow healthy bowel flora to proliferate and thrive are often called prebiotics. They are also known as resistant starches, because they are resistant to human digestion. I recently had a client call the addition of resistance starch to her diet, “the missing link my body needed”.

A starch that resists digestion and reaches the large intestine becomes food for the healthy bacteria in the large intestine. These bacteria can break down and “feed on” the resistant starch thus providing the friendly bacteria with the fuel they need to survive.

Imbalance of the quantity and type of bacteria species present in the gut contributes to gastrointestinal illness, blood sugar imbalance, obesity, mood disorders, and immune system challenges.

Green unripe bananas and plantains are one of best sources for prebiotic fiber content with 27 to 30 grams of fiber in one medium banana. Green bananas are essentially inedible. They are most easily incorporated into diet by blending into a smoothie.

One mistake frequently made incorporating prebiotic fibers from bananas is consuming bananas that are too ripe. Once the banana ripens the resistant starch is degraded and become a digestible starch. Thus, no longer a good prebiotic fiber source. In fact, the riper the banana becomes the higher the glycemic (blood sugar) response.

It can be difficult to find bananas that are very green. I made several trips to my local grocery store to find these bowel flora champions. I find it helpful to ask the produce clerk to take a look at the shipment that just arrived, noting the day the shipment arrives, for the best chance to gobble up these green beauties.

In an effort to keep green bananas green I tried a few strategies. One that sounded promising was wrapping the end of the banana to prevent the ethylene gas, which ripens the fruit, from dissipating. You can see from the image this clearly did not work. After a mere two days the green bananas were no longer green. What I found works best is placing the green bananas in the fridge. This halts the ripening process. The skin of the banana will turn brown, which is normal, but the fruit inside is still good. I’ve kept bananas in my fridge for up to 8 days and they hold up well other than the brownish black discoloring that develops on the skin. The banana will be firm and require a knife to cut the skin off the banana.

If you’d like to learn more about prebiotics and strategies to support resolution of common gastrointestinal complaints read the recently release Cureality Guide to Healthy Bowel Flora by Dr. Davis. This guide is one of the many valuable resources available exclusively to Cureality.com members.
---Lisa Grudzielanek, MS, RDN,CD,CDE
Cureality Nutrition Specialist

Something is Better Than Nothing

2. July 2014 Amber B (0)


This past weekend I attended a fitness conference with an amazing lineup of presenters. Even after 11 years in the fitness industry, I love attending these events. I’m a lifetime student always learning more and honing my craft.

I went to a presentation by Al Vermeil about joint mobility, not knowing anything about him. To my surprise, Al was the strength and conditioning coach for the Chicago Bulls and the San Francisco 49ers the years these teams won championships in their respective sports. That’s a pretty impressive resume.

Al was a great presenter, full of fun and practical advice. During his presentation, Al said the following statement:

“Every time you miss a workout, the next one is easier to miss.”

This statement really hit home because I’ve seen this time and time again working in the fitness industry and in my own life. One workout is missed, then an entire week of workouts are missed, then it’s been an entire month of never setting foot back into the gym.

It’s easy to get thrown off your workout routine when life gets busy and days get long. So what do you do? Do you just trash your workout plan?

The all or nothing attitude is common when it comes to making health changes. Either you’re following your plan 100% or you not. I’m here to tell you that doing something is better than nothing. Doing part of your workout or a mini workout is better than missing an entire workout.

The other day I had the choice to do something or nothing. I had a full day of work meetings, video, and family commitments. Here is what happened. I did shorter variation of my joint mobility routine. I followed that with a quick kettlebell circuit of 25 kettlebell swings, 12 kettlebell overhead presses, and 12 kettlebell goblet squats. I did three rounds of this circuit. That’s it! The following day, I got back to my regular exercise routine.

Be consistent with movement and you’ll always see improvements. That’s the magic of exercise. You'll get better if you just do it.

What’s the Problem with My “Healthy” Bowl of Oatmeal?

26. June 2014 Lisa G Nutrition, Oatmeal (0)


Food manufacturers have clever ways to market foods to us. Unfortunately, many foods that have a reputation for being healthy are no more than junk food disguised as a healthy food choice. I commonly see people under the influence of a “health halo” effect. This is due to strategic marketing efforts. People overestimate the nutritional value of a food that is labeled “good for you” or they underestimate the negative impact of a food because it contains a healthful ingredient, like flaxseed or fiber. In fact, a recent study from the University of Houston found that terms on food labels such as antioxidants, all-natural, and gluten-free often are used to give an otherwise standard food a "healthy" halo, and influence consumption from the well- intended consumer.

Case in point-- oatmeal. We’ve all heard about the cholesterol lower benefits from soluble fiber contained in oatmeal. It’s blasted all over packages with a paid endorsement from The American Heart Association. However, that’s not the whole story. Most people enjoy a cup of oatmeal with one to two tablespoons of added sugar and fruit such as a ripe, yellow banana. In other words, let’s enjoy a bowl of “send my blood sugar through the roof” high glycemic oatmeal. The glycemic index of oatmeal is 55, and instant oatmeal is 83. Top that with more table sugar, glycemic index 58-65 and better yet top that with a high glycemic, ripe banana with a GI of 62.

Preparing one packet of regular instant oatmeal with one tablespoon of sugar and a medium ripe banana five days per week would result in the sugar equivalent of more than 5 1/2 cups of sugar per month!

Furthermore, the story many Americans are missing is all of that sugar intake, from their so-called “healthy” bowl of oatmeal, actually raises small-dense LDL cholesterol particles, increases blood sugar and contributes to insulin resistance, faulty gut flora, and belly fat.

How do we improve upon our bowl of oatmeal? Enjoy a bowl of hot coconut flaxseed cereal, eggs any variety of ways, or last night’s leftover salmon and vegetables.

The Cureality program provides tools, guidance, and support that does not follow the party line but rather offers nutrition solutions that address the underlying causes for proliferation of many chronic diseases.

Power in Numbers

25. June 2014 William Davis (0)


In his book, The Wisdom of Crowds, author James Surowiecki begins with the story of an ox judging competition in which 800 people—not ox experts nor breeders, just ordinary people attending a county fair—were asked to guess the weight of the ox. The competition was conducted by a scientist, Francis Galton, who held a low opinion of the intelligence of the average person, remarking that “the stupidity and wrong-headedness of many men and women being so great as to be scarcely credible.” He hoped to prove, by examining the various guesses, that the average person had no idea of how to judge the real answer. After all participants casted their written votes, Galton tallied up the total and averaged the result: 1,197 pounds—just one pound off from the real weight of 1,198 pounds. Few individuals actually guessed the correct weight themselves but, when the opinions of many were combined, the result was near-perfect.

Crowds can also be a source of irrational behavior, panic, and stampede. Witness any modern football or soccer game, for instance, in which fights break out over an issue as minor as a disputed call or a heckle. Or go back through history to the countless events when mass hysteria ruled, such as the Salem Witch Trials or Orson Welles’ War of the Worlds radio broadcast.

Let’s put aside examples of mass emotional chaos of the sort that causes crowds to stampede store doors on Black Friday. Let’s focus instead on conscious, considered, thoughtful opinions. We all accept that there are as many opinions on issues as there are people, not uncommonly with widely divergent views. But can we, as Galton’s famous experiment did, combine the opinions of many and come away with some fruitful insight—the correct answer? Just as the people participating in Galton’s experiment were not experts, so Cureality participants—a crowd-sourced collection of opinions—are not experts. If we were to poll everyone to identify their area of expertise or experience, it would likely include finance, the retail industry, raising children, or teaching—but not health. Yes, we have experts curating the direction of content, but we also crowd-source collective opinion.

Right now, Cureality is based on existing science, the philosophy of self-directed health, combined with guidance and community to help the participant along in the sometimes complex world of health questions. But as our processes and procedures improve, can we—like Galton’s ox weight guessers—come away with coalescent wisdom, answers to our health questions, near-perfect solutions to health conditions that have eluded the “experts” for centuries?

I think that we can. No, I know that we can. We enter a new age in information and harness the power of the crowd-sourcing of solutions, even when no single individual has the complete answer herself.

Use This Trick to Boost Exercise Motivation

23. June 2014 Amber B (0)


Are you been struggling to get your workouts in? 

Do you belong to a gym and find that you're not going?

Do you have exercise equipment sitting in your basement collecting dust because you find that you just can’t get yourself down there?

If you answered, “yes” to any of these questions you are not alone. Many people struggle with finding the motivation to exercise.

The problem here is that you have head trash going on. Head trash is that voice inside your head coming up with a million excuses that inhibit you from carving out a bit of time to take care of yourself.

Head trash will tell you that you’re too tired, even though a workout would give you a boost of energy.

Head trash will tell you that you’re too busy, even though you just spent a half hour on Facebook.

Head trash is barking at you to take care of others, even thought you know your health is important for you well being.

Head trash is a real conflict that can get in the way of our health and fitness goals. We start an exercise program with the intentions of a long-term commitment. But after the initial excitement wears off, we find our workouts occurring less frequently. Head trash begins to take over and soon we find ourselves not exercising at all.

Here is my secret for winning the battle over the head trash that keeps getting in way of your workouts. Tell yourself that you are only going to exercise for 10 minutes and evaluate if you want to continue. If you're truly too tired you can stop after 10 minutes. If you're truly too busy you can stop and move onto a task that needs your attention.

Making this deal with your mind that you are only going to exercise for 10 minutes seems reasonable. The head trash will become quite because your mind is convinced it has an out within 10 minutes.

I've used this 10-minute trick myself. I grind through the first few minutes, but then the magic happens. Once you hit the 10-minute mark your body takes over. Exercise feels amazing and your body is energized and enjoying the movement. You have tricked your mind to get over the hurdle of starting and now you’re in the exercise groove.

Try the 10-minute trick next time your head trash is getting in the way of your workout. You'll be amazed how your workout consistency improves.

The exception to low-carb

The exception to low-carb

31. July 2011 William Davis (60)
I witness spectacular results restricting carbohydrates, both in the office as well as in my online experiences, such as those in Track Your Plaque. Of course, the diet I advocate is not just low-carb; it starts with elimination of wheat (for a long list of reasons). So the diet is wheat-free in the setting of low-carbohydrate.

What does this accomplish? Here's a partial list:

--Weight loss-Specifically, loss of visceral fat, the kind hinted at on the surface as "love handles" or what I call "wheat belly."
--Reduced blood sugar and HbA1c (reflecting prior 60-90 days glucose)
--Marked reduction in small LDL and triglycerides, increased HDL
--Reduced inflammatory measures like c-reactive protein
--Reduced leptin and leptin resistance, increased adiponectin
--Reduced estrogen and prolactin in men, accompanied by shrinkage or loss of enlarged breasts ("man boobs"); reduced estrogen in females accompanied by reduced risk for breast cancer

Pretty impressive. But there's one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.

Everybody has two genes for apo E; the most common type is apo E 3/3. Around 1 in 4 people have 1, less commonly 2, genes for apo E4.

I hate apo E4. I hate apo E4 because it means I've got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that's what apo E4 people have to do. But it doesn't end there.

Apo E4 people also typically have plenty of small LDL particles triggered by carbohydrates. Put fats and carbohydrates together and you get an explosion of small LDL particles. Remove fats, small LDL goes down a little bit, if at all. Remove carbohydrates, small LDL goes down but total LDL (mostly large) goes up. The large LDL in apo E4 does seem to be atherogenic (plaque-causing), though the data are fairly skimpy.

So apo E4 creates a nutritional rock and a hard place: To extract full advantage from diet, people with apo E4 have to 1) go wheat-free, low-carb, then 2) not overdo fats, especially saturated fat.

It still gives me the creeps to tell an apo E4 person that they've got to watch their fats, worse than watching Starsky and Hutch reruns.
Tags :

Comments (60) -

  • Simon

    7/30/2011 10:45:35 PM |

    What does one eat if they are wheat free, low carb, and low saturated fat? Can anyone give a sample day for this plan?

  • Paul

    7/30/2011 11:44:42 PM |

    Have you tried T4/T3 adjustments with apo E4?

  • PeggyC

    7/30/2011 11:48:10 PM |

    How can one find out if one has Apo E4?

  • steve

    7/31/2011 12:38:22 AM |

    Is it possible to have the same reactions to fats such as large increase in LDL, mostly large with little small LDL?  At one point i was 100% small LDL; restrcting carbs and increasing fats of all kind(good ones only) my NMR was 2098 LDL of which 200 were small were small.  HDL was 69 and TRGs 62.  Only way to get these numbers down is to be on statin and zetia.  Thought i was an ApoE 4, but test showed i am ApoE 3/3.
    Perhaps i am a hyper-absorber of fats- maybe as bad as ApoE4?   With statin and zetia i can reduce the numbers to LDL total of 640 and <90 small.    So maybe the high fat diet is not so great even for those who are not ApoE4.
    Thanks for your thoughts.

  • Buckaroo Banzai

    7/31/2011 5:19:21 AM |

    I'm getting my ApoE status tested soon.  I've been quite liberal with the healthy fats (olive, avocado, pastured eggs) and include saturated coconut oil and dark chocolate.  I also have high LDL particles - about 1500, but only 139 are small without statins.  I would love to find out I am 3/3 because I've already restricted grains and a variety of foods that I tested as allergic too including nuts.  I asked Dr. D on the forum if having <10% small particles was good news, but he was still worried about the total LDL.  I guess we will see how worried I should really be shortly.  BTW, I've got high Lp(a) at 26mg/dl, so I really don't need another strike against me in my plaque battle.

  • Might-o'chondri-AL

    7/31/2011 6:35:43 AM |

    Lost a nice technical ApoE explanation  I spent a lot of my time on to "server error" .
    I'll just lurk from now on.

  • Renfrew

    7/31/2011 12:46:17 PM |

    Mighto:
    Please stay here and enlighten us with your comments. Glitches can happen. I made it a habit a long time ago to just copy my text (Ctrl.A, Ctrl. C, on WINDOWS) before sending it. It is easy and takes no time. Text is preserved and you can try again.
    I for one am enjoying your musings tremendously.
    Cheers, Renfrew

  • Beth@WeightMaven

    7/31/2011 2:17:43 PM |

    What Renfrew said. I've run into this problem on blogger regularly where it decides to log me off while posting a comment. Now I always save any longish comment before posting. Better safe?

  • Jolly

    7/31/2011 2:26:04 PM |

    Digging into my 23andMe data, it reports back on APOE e4 status Smile

    You can find this as part of the https://www.23andme.com/you/journal/alzheimers/overview , or just check the rs7412 & rs429358 SNP's directly.

  • Gene K

    7/31/2011 3:39:12 PM |

    I am an APOE 3,4, and here’s what I eat on week days.
    Breakfast.
    Steamed raw vegetables (eggplant, zucchini, bell peppers, mushrooms, Mexican or yellow squash). Add yellow mustard and dry spices.
    Natto twice a week (1 box Mito natto, throw away their soy sauce and mustard packages).
    Frozen blueberries (1/8 cup), 3 tbsp flaxseed meal, 1 cup unsweetened almond milk - all microwaved for 2 min. Add ground cinnamon.
    Half-ounce piece of part skim milk mozzarella cheese.
    Coffee.
    Lunch.
    Frozen vegetables (California blend – cauliflower, broccoli, carrots) microwaved (reheat). Add a boiled egg, 1/4 avocado, yellow mustard.
    Dinner.
    Cooked or baked vegetables (cauliflower, bok choy, green cabbage, rapini).  
    Sautéed or baked fish (tilapia, salmon, perch, trout), chicken breast, or ground turkey meat balls. Add yellow mustard, horseradish, and dry spices.
    Generous amount of raw vegetables (green lettuce, pickles, tomatoes, bell peppers) with hummus.
    Decaf tea with a 1/10 serving piece of 90% dark chocolate, half-ounce mozzarella cheese, and some almonds or sunflower seeds.

  • Gene K

    7/31/2011 3:43:03 PM |

    My daily fruit serving includes a cup of frozen dark berries (blueberries, raspberries, blackberries) from the Costco Three Berry bag.

  • mallory

    7/31/2011 4:18:37 PM |

    back incollege i did a report on cancer and ottowarburg and i remember this gene being incredibly linked to cancer risk....any truth to that?

  • Dr. William Davis

    7/31/2011 4:48:42 PM |

    Hi, Steve--
    There are indeed genetic predispositions outside of apo E4 that can provide for this response, e.g., apo B receptor variants. What is not known is when you've crossed a threshold of mostly or purely large LDL that is undesirable. Despite $2 billion spent on statin drug-related research, we still have no answer on this question.

  • Dr. William Davis

    7/31/2011 4:50:18 PM |

    Hi, Buck--
    Similar issue as the question posed above by Steve: We just don't know what an "allowable" quantity of mostly or purely large LDL particles are. For a working value, I've been trying to keep NMR-derived LDL particle number 1500 nmol/L or less when LDL is purely large, but I have no endpoint data to justify this.

  • Dr. William Davis

    7/31/2011 4:51:22 PM |

    Great program, Gene, given your pattern. And I am impressed at your courage to eat natto!

  • Dr. William Davis

    7/31/2011 5:06:39 PM |

    Hi, Mallary--

    Hardly my area, but I believe that the relationship between apo E4 and cancer in various sites is complex and modulated somewhat differently than in other apo E genotypes. Some discussion:
    http://aje.oxfordjournals.org/content/170/11/1415.long

  • Dr. William Davis

    7/31/2011 5:08:35 PM |

    Hi, Simon--

    The full diet is articulated in detail, including scientific rationale, in several reports on the Track Your Plaque website; link above. Chapter 9 of the New Track Your Plaque Guide is also devoted to this.

    As you see, I will be putting out recipes here and on the Track Your Plaque website in coming months.

  • Might-o'chondri-AL

    7/31/2011 7:28:48 PM |

    even 1 reconstructed paragraph just  lost to "server error"

  • Might-o'chondri-AL

    7/31/2011 7:33:54 PM |

    ApoE joins with ApoB and is carried in VLDL and chylomicrons; it is ApoE that binds to tissue cell LDL receptors to start normal uptake. Inside the ApoB with lipids breaks off and heads into tissue cell lysosome.
    Meanwhile ApoE and the LDL receptor head back to that cell's membrane, with ApoE carrying some cholesterol out of that cell to build into an HDL molecule for recycling.

  • Tim Dietz

    7/31/2011 8:32:10 PM |

    I have the worst of both worlds, I think, as I am E2/E4.  Dr. Davis, do you have a specific program for patients with this genotype?

  • Tim Dietz

    7/31/2011 8:49:56 PM |

    So, Gene, I'm curious.  It looks like you have an extremely low intake of protein.  How are your labs and what kind of activity do you do during the day?

  • Gene K

    8/1/2011 4:13:05 AM |

    Eggs, natto, fish, poultry, and nuts are all rich in proteins, correct? I increase my portions of fish and poultry when I go to gym. I also add canned fish on these days like tuna in water or sardines in mustard sauce. I used to consume large amounts of tofu, but stopped recently based on some negative information I learned from a TYP member forum.
    Every weekday I typically walk to and from the train station, 25 min each way. I work out two or three days a week following the slow burn routine; I do cardiovascular, too. I also ride my bike for 2 hrs every weekend.
    I am a software engineer, so I spend most of my business hours in front of a computer.
    Before I learned about my APOE 4, I used lots of olive and canola oil and was a vegetarian, but had already reduced carbs. My labs were pretty bad and actually much worse than when I ate lots of bread and oatmeal every day. In mid-December 2010, I started eating as described above plus taking niacin (500 mg) and Crestor (10mg). I was already taking the standard TYP supplements – vitamin D3, fish oil, iodine. At the end of March 2011, my NMR was the best I had ever had: LDL-P 568, LDL-C 70, HDL-C 55, Trig 24, HDL-P 29.5, Small LDL-P 293, LDL size 20.4, HDL size 9.7, Large VLDL-P 0.7, insulin resistance 16. I don’t have genetic lp(a). I know the results can be better, so I am looking forward to my next NMR due in the fall.

  • TimK

    8/1/2011 7:34:36 AM |

    I'm confused. When you say 1 in 4 have this gene are you saying it's a *problem* in 25% of everyone? As in one-quarter of us should be eating like Gene K (above)? Or is a case where the gene isn't always active or something?

  • Dr. Jack Kruse

    8/1/2011 12:21:31 PM |

    I recently wrote about Alzheimer's on my blog and this question came up in the comment section.  I think about APoE4 completely differently than you do and here is why.  APoE4 confered humans the ability to migrate out of the sahara and north and south to live in climates with less solar radiation.  It allowed us to live with lower vitamin D levels.  Moreover, its presence alone means nothing unless it is accompanied with the epigenetic triggers that make it dangerous.  Dr Davis you and I both know the disease you treat (heart disease) and the one I treat (Cerebrovascular disease) are the same disease just found in different organs.  SO i think we have a lot in common in what we do but how we think about thi sissue is different.  Here is my take.  I posted this answer on another forum and I think it needs to be discussed here.

    I think the ApoE4 story is an interesting one and one I briefly touched upon in my AD blog.......I will revisit it.......but ultimately I dont think it is that important if you live an optimal life from 20-60. ApoE4 means much if you make poor epigenetic choices. I think people who come here do do what the rest of America does.

    The other reason I think it means little is the epidemiology of ApoE4 in those over 80 yrs old. It does not have any major impact on healthy aging once you get to old age. That tells me that the epigenetic signals need also be present for it to matter.

    ApoE4 is like dynamite.......and high insulin and high PUFA consumption and lowered total brain cholesterol (due to altered lipid uptake) are the major lit matches. If they exist by themselves they are harmless......but if they are brought together you are going to get heart disease and AD early and get taken out.

    Dr Kruse

  • Peter Silverman

    8/1/2011 6:24:50 PM |

    So everyone who is eating or planning to eat a high fat diet should get tested for E4, or are there some things that indicate it's probably unnecessary?

  • Jack Kronk

    8/1/2011 8:12:52 PM |

    Dr Kruse -

    It's pretty scary for me to think that maybe I am not supposed to be eating very much saturated fat. If it's true that is unbelievably lame. This is why I'm thinking I need to check to see if I am ApoE4. (How do I test for that?) If I am, then it may explain why, even on a Paleo diet, my LDL is mostly small dense. Are you suggesting that if I keep PUFA very low, like cut out my only remaining source (almonds/pecans), that this could be a key to producing more pattern A LDL? (By the way... I have chosen to eliminate all nuts and nut butters, regardless).

    -Jack Kronk

  • Patri Friedman

    8/1/2011 8:58:31 PM |

    Thanks so much for the thoughts - I am an E4/E4 eating a Paleo 2.0 diet.  As I understand it, high-protein is not a healthy diet, so low-fat & low-carb is not a good idea.  Fat is the healthiest macronutrient, so I'd love your opinion on which types of fat are best for E4s.

    It sounds like you have concerns about saturated fat, and of course I avoid n-6 PUFAs and get lots of n-3s from grass-fed animals & fish oil.  What about coconut oil?  Olive oil?

    What sort of HDL/LDL/etc  numbers would you look for in an E4/E4 as warning signs?  As health signs?

    BTW, I blog occasionally on APOE4 at primale4.wordpress.com, am going to quote your post there.

  • Tim Dietz

    8/2/2011 1:42:49 AM |

    Thanks for that, Gene.  I may need to go your route with my profile.  I'm following TYP pretty religiously and am having my 6-mo labs this month, so hopefully they will be improved from last time.

  • Dr. Jack Kruse

    8/2/2011 3:51:19 AM |

    Jack as I mentioned to you on my blog I think you clearly need context.  I think your epigentics are telling you something.  But here is what I cant tell you and neither can anyone else.......without testing!  You need to be tested to get that context.  I think your diet you posted gave many clues......but even I did not jump to the easy conclusion.  I think your real underlying issue is multifactorial but your VAP strongly points to a leaky gut as a source of the sdLDL.  I think the bananas and cream are problems too.  Your O6/O3 ratio maybe bad and yes......you may have a bad set of allele's for ApoE4......but guess what!  Your HS CRP was very very low.  This tells me that your match is not lit.  So you may only be carrying a stick of dynamite.  Again......carrying dynamite is not going to blow you up.  This is why you need testing to get more context.

  • Dr. Jack Kruse

    8/2/2011 4:05:59 AM |

    We send our ApoE4 patients to an nearby academic lab for testing.  One is likely available in your community because cardiologist and neurologist are ordering this test quite often now.  I think your PUFA content of your diet and of your tissues is critical.  In fact for AD the PUFA content is a major factor.  I believe it is a huge factor for CAD disease as well.  Wheat, Carbs, and PUFA's all drive sdLDL production.  Its not just one part of the diet that does it.  Moreover, the more leaky the gut the more sdLDL one will have as I laid out in my VAP blog that I dedicated to yourself.  I think your case is quite representative to many thousands of people and I am glad we are talking about it here because Dr Davis is a cardiologist and is coming at this issue from a different angle than I am.  I think however when the story plays out.......we will be in the same neighborhood because human biochemistry pathways are constant.  The fuels and hormone status and the situations in our guts are the covariables that make this issue more confusing.  I think people need to know why Apoe4 is important.  It conferred an adaptive advantage to move away from the equator to lower solar radiation and lower vitamin D levels.  This adaptation is seen in many american african americans.  The other interesting finding is that the liver of these patients makes more cholesterol to try to raise the D level and pregnenolone level to offset the deficit.  It never does.  But when this set of circumstance is mixed with a high carb low fat SAD (PUFA rich) it destroys the heart, vessels and brain.  This is what we see today in many parts of the world.  Their diet is now completely mismatched for the original adaptation.  I think if you tweek the diet when you know the epigenetic variables you can easily over come an Apoe4 positive test if youre willing to change.   But you need to test!

  • Dr. William Davis

    8/2/2011 11:01:58 AM |

    Hi, Tim--
    Very rare, as you likely know.
    I believe that you simply deal with this on a practical level, i.e., deal with the small LDL and insulin resistance issues and postprandial abnormalities from apo E2 as you ordinarily would. Then deal with the LDL-accumulating aftermath from the apo E4 component.

  • Dr. William Davis

    8/2/2011 11:07:23 AM |

    Thanks for the insightful thoughts, Dr. Kruse.
    I'm not sure how your approach folds into mine, though fascinating. I do agree that apo E4 is made much worse by the means you cite, i.e., polyunsaturates, carbohydrates that trigger small LDL. This is why, despite the LDL-accumulating effect of apo E4, I focus first on reducing the small LDL component, in effect an anti-inflammatory, glycation-reducing, oxidating-reducing approach, followed only then by dealing with any large LDL-increasing aftermath.
    What is not clear to  me is how atherogenic the large LDL is at higher levels in the setting of apo E4. As you know, one of the greatest concerns in apo E4 is that its effects may not be confined to lipid effects, but may extend into non-lipid effects. But that is such poorly charted territory.

  • Dr. William Davis

    8/2/2011 11:12:52 AM |

    Hi, Patri--
    The formal data on the various fat fractions and apo E4 are, unfortunately, very skimpy.
    Saturated fat clearly increases whatever LDL dominant form there is. However, other forms of fat, even omega-3 fatty acids, also increase apo E4. This become a problem, for instance, when we try to use high-dose omega-3 fatty acids to reduce Lp(a) in the presence of apo E4.
    As I commented above in response to Dr. Kruse's comments, as a practical matter I believe it is best to address the worst fraction of LDL particles first, i.e., take dietary steps to reduce small LDL particles, meaning reduce carbohydrate triggers of small LDL. Then deal with the large LDL that emerge by varying fat intake and gauging effect.
    Odd thing: Even among apo E4 people, fat intake yields variable LDL-increasing effects, quite variable sometimes.
    Also, recall that health extends beyond LDL. So there may be benefits to monounsaturates or omega-3 polyunsaturates, say, that extend to issues like brain and liver health.

  • Melinda

    8/2/2011 2:57:02 PM |

    Hi Melinda,
    Please copy and post this in previous thread for ApoE4 … .
    Continuation about ApoE4:
    % of ApoE4 messes dynamic inside tissue cell so that ApoB turns to use Scavenger Receptors to try to start cascade which gets signal transducer (Specificity Protein 1) to up-regulate the cell membrane transporter protein ( ABCA1, ATP binding cassette transporter A1) that puts excess cholesterol out from that cell. I believe this is where Doc Davis’ stated ApoB irregularities add to the problem with ApoE4 (since normal human ApoE3 works all by itself to get that signal transducer to bind to ABCA1 to work shucking cholesterol) . When cholesterol gets to build up inside the cell the large LDL can acetylate and form excessive “droplets” in that cell’s cytoplasm; while the small LDL can oxidize from CuSO4- and load up inside that cell’s lysosome.

    Meanwhile % of ApoE4 doesn’t just dock with tissue cell LDL receptors and so the macrophage scavenger receptors pick up too much cholesterol laden ApoB/ApoE lipo-protein carrier molecules. Once in the macrophage the same problem of oxidized LDL piling up in lysosome and acetylated LDL burdening cytoplasm occurs; and for that matter, in macrophages, it is down to ApoB to get the signal transducer going if any cholesterol is to be put out by cell membrane transporter protein ABCA1. This is the recipe for risky pro-atherogenic “foam cell” formation; while the individual genetics of ApoE, ApoB, assorted receptor types, signal transducer and transport protein all make it hard to predict how ApoE4 plays out.

    Dr. Kruse broaches ApoE4 in alzheimers and this is in large part because ApoE4 causes the brain neurons to get less than optimal cholesterol from the brain’s astrocytes. It is ApoA1 working in HDL complex that controls the astrocyte cholesterol balance and when there is inflammation there is a risk of ApoA1 mis-folding to foster amyloid aggregations. Low intact ApoA1 and ApoE4 together increase the risk factor for cognitive problems and dementia several fold.

    Diabetics with ApoE4 have that % of ApoE4 as an additional limitation; however, irregardless of the ApoE iso-form diabetic dementia risk arises from their glucose loads impairing kidney tubules, and thus fostering the uremic environment that stymies ApoA1 bio-synthesis. The normal role of ApoA1 is to bind to the transport protein which secures cholesterol into a safe bond with HDL; so low ApoA1 from any factor will challenge the brain neuron over time. I suggest there are individuals whose age impaired kidneys contribute to senile dementia from impairing ApoA1 levels being made and also possibly speeding up the normal 4-6 days kidney elimination of ApoA1 ; and so Patri’s comment on limitation of high protein intake is relevant due to it’s demand on aging kidneys.

    Reply

  • Melinda

    8/2/2011 3:01:05 PM |

    The above comment was written by Might-o'chondri-Al.  He asked me to post it in this thread as he is having trouble posting here.

  • Jack Kronk

    8/2/2011 4:52:20 PM |

    Ok I will test! But I have been asking around how to test and still don't know how? Is this something that I would just ask my doctor about? Maybe I go to the same lab that did my VAP? Since I got my results 3 weeks ago, I have made the following changes: zero bananas, reduced my cream intake by about 70% or so, lowered my overall fruit intake signigicantly, added 2 teaspoons of red palm oil daily, decreased caffeine intake (and now I am doing no coffee in August). I have also decided to eliminate all nuts and nut butters as of 2 days ago. Now my only real source of PUFA left in my diet is bacon, occassional chicken, and avocado. It's weird too, because on SAD, I was probably getting 10 times the PUFA, at least. I cooked in canola, ate loads of grain bread and corn products like tortillas. Maybe adding the saturated fats makes everything more amplified. The only thing now that I am VERY reluctant to give up is starches like potatoes and white rice. If I do, I will surely be VLC again, as I don't eat breads and very little fruit now, and rarely ever indulge in sweets. This means, by default, that most of my calories would then be sat and mono fats. Isn't that not good if I am ApoE4? What a mess! Dr Davis is right about being between a rock and a hard place. Jeez!

  • Jack Kronk

    8/2/2011 5:01:51 PM |

    "high protein is not a healthy diet". you mean specifically for ApoE4 folks? I haven't been tested for it yet, but I suspect I may be ApoE4. I take whey protein daily and eat lots of eggs and beef. I do this on purpose because I do weight training 5x per week and am building muscle. Could it be true that people who are ApoE4 are not supposed to build much muscle? (logically speaking, due to the restriction on protein)

  • Might-o'chondri-AL

    8/2/2011 5:20:02 PM |

    Is server cooperating now ?

    ApoE4 degrades more readily than ApoE 3 or ApoE2; ApoE4 protein fragments that get into a tissue cell's cytosol can have bad effect on that cell's mitochondrial membrane lipid binding . This decreases the mitochondrial efficiency  when they try to perform glycolysis for generating energy.

    ApoE4 degradation in a cell cytosol can  decrease the level at which that cell advances it's bio-genesis of  robust mitochondria; this is due to how ApoE4 fragments depresses PPAR gamma expression & PPAR gamma is what promotes making good mitochondria. (Specificly in the case of human fat tissue PPAR gamma is what regulates transcription of pre-adipocytes differentiation into true adipocytes. Hence Avandia & glitazone drugs that target the receptor of PPAR gamma do short out adipocyte differentiation;  and yet risk the side effect of increasing heart disease due to mitochondrial impairment.)

    In Alzheimers the form of ApoE makes a difference; and the brain amyloids react to insulin differently with different ApoE iso-forms. The ratio of insulin in cerebro-spinal fluid as compared to insulin in plasma changes with different genotypes of ApoE.   Alzheimer patients tend to have lowered glucose utilization in their brains with  less insulin and insulin-like growth factor receptors, despite the Alzheimer brain harboring fewer insulin degrading enzymes. Which engenders a paradox whereby diabetic brain neuro-pathy experimentally improves with administration of nasal insulin; and similarly,  individuals  with ApoE4  receiving nasal insulin improved their cognitive function, with the boost being higher in ApoE4 carriers than folks with any other alleles of ApoE.

    Higher amounts of Alzheimer amyloid  formed tangles are seen in Type 2 diabetics and in those with ApoE4; leading to the conclusion that "normal" ApoE3 fortuitously forms a complex with brain amyloids.
    Apparently ApoE iso-forms other that ApoE4 can more readily bring an amyloid to where the molecule LRP-1 (lipo-protein related protein 1) can move that amyloid out across the brain blood barrier .

  • Might-o'chondri-AL

    8/2/2011 5:31:26 PM |

    Hi Melinda,
    Thanks for repost, looks like Doctor D hammered his server into shape again.

  • Dr. Jack Kruse

    8/3/2011 4:57:17 PM |

    With regards to the large LDL content.  Again I am not a cardiologist, but a neurosurgeon.  The heart and brain work on the same principles of biochemistry.  And since these two organ take up much of the CO in the body they share much in common.  It is also why when we see neolithic disease affect the heart their is also a similar effect in the brain.  The Apoe4 story is one such case.  But so is the large LDL story.  Cardiology CW today believes that LDL matters.  In neurosurgery today its clear in neurodegenerative disorders we are lacking LDL and cholesterol more often than not.  This is incongruent to biochemistry.  Dr davis has said here in this thread the jury is out on large LDL in his field.  I am submitting that LDL matter little in any field.  Why?  If it did the body would have a specific detailed regulatory control method in place to deal with it and it does not.  In nature, with the consumption of organic, unprocessed parent essential fats rather than adulterated oils (PUFA's) and transfats, LDL cholesterol is supposed to be made up of significant amounts of properly functioning “parent” omega-6, linoleic acid (LA), and is not supposed to be harmful. It is the natural transporter of parent omega-6 and parent omega-3 into the cells. It is thus not critical to lower LDL cholesterol, nor is the absolute LDL number as important, if the diet contains sufficient unadulterated parent essential fats. These are unadultered PUFA's of both the omega 6 and 3 variety for clarity sake.  Also take note that the body has no natural “cholesterol sensor” in the bloodstream—it would if its levels had to be maintained within exact limits; such as, sodium, calcium, and glucose levels are monitored in many systems. For example, glucose levels are maintained to an amazingly tight 0.1% in each of us!  So Nature implemented biological mechanisms if required. There is no need for a cholesterol sensor because the absolute number is irrelevant.  That was my advice to Jack Kronk three weeks ago when he posted his VAP numbers and when I blogged about his numbers.  I understand that Dr Davis may not want to go out on a limb as I have here.  But I dont view it as a limb when the biology and biochemistry support my beliefs fully that LDL cholesterol levels are completely irrelevant to heart disease propagation.  This is why I advocate copious amounts of coconut oil to patients with heart disease and all neurodegenerative disorders including brain tumors and seizure patients.  In fact, my literature is loaded with thousands of papers supporting my belief made here.  I think its long over do that cardiologists start reading "other pathways" of data to reach conclusions that their own field muddies.  As a neurosurgeon, I read Dr Davis literature quite a lot and in comparing the two it is clear that our two fields are on a collision course from two different paths.  I got extreme clarity reading circulation over the last thirty years that cholesterol has nothing to do with heart disease.  Dr Davis has reach conclusions that are quite different from most of his fellow cardiologist as well.  I applaud him.  I just think he is still caught in the lipid hypothesis nightmare and that is the only reason he is not traveling down the road with me in unison.  Since he is a fine doc and one who clearly is ahead of his peers......i'll gladly wait for him on that road because we need him to alter what ails his branch of medicine to get to where we both need to be going for all patients.

  • Davide

    8/4/2011 2:24:29 AM |

    Dr. Kruse,

    What is your response to the fact that people with familial hypercholesterolemia (FH) have an exaggerated risk of CVD versus those who are not lacking ldl receptors? Why do so many of them have cardiac events in their 20's and 30's? Surely, you would not relegate this phenomenon to increased consumption of PUFA's and/or higher insulin?

  • Dr. Jack Kruse

    8/4/2011 4:21:16 PM |

    There are five major classes of FH due to LDLR mutations.  FH is a collection of genetic defects.  Many believe that the end result of these defects (IE high LDL or cholesterol) cause the diseases associated with it.  I do not.  Why?  When these people live past their 6th decade they have extremely low levels of neurodegeneration.  I believe the cause of the early on set  CAD is tied to secondary effects of what the primary genetic disease does to the liver to alter its function.  If one looks at FH patients and their VAP results one sees a pattern of chronic gut inflammation that is the real source of the atherosclerosis that causes higher incidences we see in FH.   These patients all have altered gut biofilms and some of the lowest levels of Vit K2 and vit D.  They also have extremely low DHEA S and pregnenolone levels are pointing to a chronic inflammation......due not to the high cholesterol level but to an altered gut axis.  Read my blog on this here.    http://jackkruse.com/your-vap-brain-love-not-war/   My views on this topic are radically different because even with severe LDL lowering treatments the disease patterns these people face remain unchanged.  Why?  because their gut remains the source of the inflammation that damages their arteries for their entire life.  We need to focus our efforts on the gut side of the equation and not the LDL side.  Ironically Dr Davis has done this with his assault on wheat.  Wheat drives sdLDL via what mechanism?  It screws up the liver and increases gut permeability to cause issues.  His current ideas and mine are very close.......but no one is tying this together.  I think my VAP post on the gut provides you the link.

  • Might-o'chondri-AL

    8/4/2011 10:55:40 PM |

    Genetic high total cholesterol is related to the over 50 amino acid variations of PCSK9 (pro-protein conertase subtilisn/kexin 9,  which comprises 692 amino acids). Individuals producing an excess of PCSK9 more extensively degrade their cholesterol receptors with surface defects; and so don't readily take up LDL out of circulation, which lets blood levels of LDL rise higher. Conversely, those making sparse PCSK9 can't degrade their LDL receptors, which pull lots of cholesterol into a tissue cell where it can pile up over time in that cell's lysosome; and blood levels of LDL seem to drop.


    PCSK9's worst version is D3744; where total cholesterol trends to 4 times normal and risk of death is estimated to be even +/- 10 years sooner than even other problematic PCSK9 genetic variations that affect maybe 1 in 500 westerners and account for +/- 5% of all pre-mature coronary heart disease. As regards the "older" age survival ability of those with familial high cholesterol  this may be due to the way over time plaque holds less lipid content and acquires more collagen with calcium infiltration. In other words younger plaque is less stable and more likely to burst free and be perilous.

    If fretting about plaque be aware that the average duration of carotid plaque is +/- 9.6 years; according to Carbon 14 dating from autopsies. Plaque may even form multiple times during one's life and the statistically dangerous symptoms take 5 - 15 years to manifest. Increased levels of circulating plasma insulin accelerate the rate that plaque forms; and also adds to a plaques instability (ie: potential to rupture) due to insulin's interaction with genes involved in the immune response;  like how those with insulin resistance make more pro-inflammatory cytokines. This bolsters Doc Davis' insistance to control glucose, since the down stream result is a more stable plaque.

    Noteably, there is the so called "protective cytokine" TGF beta which can allay plaque rupture. This is hard to predict for individuals because we have no way to assess who has what types of TGF beta receptors around , since normal and then plaque ridden blood vessels can harbor different TGF beta receptors. TGF  is considered a vital player inside vascular smooth muscle cells because it forms part of the interactive sequence that stops the smooth muscle cells from altering; and it bears mentioning that excess cholesterol can inhibit some TGF beta pathways.

  • jegesq

    8/5/2011 4:28:04 AM |

    For those who asked (Jack Kronk, Peggy, et.al.) about where and how one can get tested for ApoE it's simple:   Virtually any large commercial lab in the U.S. can do the test, e.g., Labcorp, Quest, etc.   Also, Atherotech (VAP) and Berkeley Heart Labs will do the test as well.   Since it's a genetic test, it's only run once during a person's lifetime.  The test can run anywhere from around $100 on up, depending on which lab runs it for you.

  • Dee

    8/5/2011 1:49:05 PM |

    In my last lipotropen test, I do not absorb chol not do I make it.  Am I a closed system?  My lp[a] is 41.  I am very puzzled.

    Dee

  • Dee

    8/5/2011 2:20:34 PM |

    That was from the Boston Heart lab.  I am a AP03/3.

  • George Zachary

    8/6/2011 12:21:32 AM |

    Super interesting!

    Do you know what SNP is PCSK9 ?  I'd like to look up it in my 23andme info.
    Thanks,
    George

  • Dee

    8/6/2011 12:29:15 AM |

    Plasma PCSK9 levels correlate with cholesterol in men but not in women
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    $ 41.95


    References and further reading may be available for this article. To view references and further reading you must purchase this article.


    Janice Maynea, , , Angela Raymonda, Anna Chaplinb, Marion Cousinsb, Nadine Kaefera, Charles Gyamera-Acheamponga, Nabil G. Seidahc, Majambu Mbikaya, Michel Chrétiena and Teik Chye Ooia, b

    aHormones, Growth and Development Program, Ottawa Health Research Institute, The Ottawa Hospital, University of Ottawa, Ottawa, Ont., Canada

    bClinical Research Laboratory, Division of Endocrinology and Metabolism, Department of Medicine, The Ottawa Hospital, University of Ottawa, Ont., Canada

    cLaboratory of Biochemical Neuroendocrinology, Clinical Research Institute of Montreal, Montreal, Que., Canada

    Received 29 June 2007.  Available online 18 July 2007.

    Abstract
    Proprotein convertase subtilisin kexin-like 9 (PCSK9) is a secreted glycoprotein that negatively regulates low density lipoprotein receptor (LDLR) levels. Several single nucleotide polymorphisms (SNPs) in PCSK9 have been linked to autosomal dominant hypercholesterolemia (ADH). Conversely, hypocholesterolemia associates with both ‘loss of function’ nonsense and missense SNPs in PCSK9. We examined the association of plasma PCSK9 with lipoprotein parameters in 182 normolipidemics. For men (n = 98) plasma PCSK9 averaged 6.08 ± 1.96 μg/ml and Spearman analysis revealed significant correlation between it and total cholesterol (TC), LDLC, and TC/high density lipoprotein (HDLC) (r = 0.276, 0.282, and 0.228, respectively). For women (n = 84) plasma PCSK9 averaged 6.46 ± 1.99 μg/ml having no correlation with TC, LDLC or TC/HDLC. The ratio of plasma PCSK9/LDLC increased in men carrying ‘loss of function’ PCSK9 variations. Our results suggest a gender difference in PCSK9 regulation and function with PCSK9 correlated to TC and LDLC in men but not women.

    Keywords: Plasma PCSK9; Loss of function; Hypocholesterolemia; Hypercholesterolemia; Single nucleotide polymorphisms

    Article Outline
    Materials and methods
    dI found this on the internet, I'm not sure if this is what you need?  

    Dee

  • Dr. K

    8/6/2011 8:27:02 PM |

    All patients with FH need to have their thyroid optimized.  This issue was hashed out at the Ancestral Health Symposium on August fifth at UCLA.  Jack Kronk's VAP is helping many patients learn how to raise their HDL to increase endotoxin clearance from the portal circulation to prevent oxidation of slow moving cholesterol because of A lack of their LDL receptor.  Thyroid optimization can overcome this to a degree but it requires a physician who knows precisely how to do this and not create an unsafe situation.  Their diets has to be a strict low carb moderate protein paleo diet high in coconut oil.

  • Dr. K

    8/6/2011 10:05:56 PM |

    This too can be assessed by looking at thyroid beta receptors......it is associated with down regulation or resistance of this specific thyroid receptor.  A company in Denmark has a clinical trial on going about this specific receptor.  Thyroid hormones bing to both thyroid alpha and beta receptors.  But disease that affect the LDL receptors seem to preferentially knock out the thyroid beta receptor.

  • Dee

    8/6/2011 11:28:44 PM |

    I apologize if I sent the wrong ifo.  Didn't read it through.
    Dee

  • Jack Kronk

    8/8/2011 2:28:15 PM |

    Dr K. -

    I am inquiring with the my Doc about getting tested for ApoE. I will let you know how that goes.

    Regarding hypothyroidism, yah the issue that I'm running into is that "it requires a physician who knows precisely how to do this and not create an unsafe situation".

    This is the problem with our medical system in America. I live in San Diego, one of the biggest, most advanced cities on earth, and I am having trouble finding anyone over here that can truly help me with this. My doctor situaiton is pathetic. Sorry to say that, but I'll call a spade a spade. All they want to do is put me on Lipitor and go low fat whole grain. So then I am stuck with doing my own diligent research, and appyling knowledge that I can learn from people who actually know what they are talking about, and right now, for me, that means the internet. Incredible when you think about it.

    When you say low carb, do you mean no starch as well, not even potatoes? By the way... the name of this post is "The Exception to Low Carb". So... that's why this is so confusing. Some very knowledgable people think it's best to raise my intake of starches and lower my fats. If my body is creating more LDL (even small dense) because of my saturated fat intake, then it makes sense to replace sat fats with something else. I already get enough protein, so then I am left with carbs. If it has to be carbs, isn't safe starch my only real option? It can't be 'sugar'. It can't be 'fructose', or grain starch, right? Should I eat loads of salads? Or I am on the wrong track completely? Should I look at upping my mono fats in place of saturated, like using mac nut oil for cooking? Or would mono fats be just as problematic?

    You see? Honestly, I know this stuff stone cold. I know what *most* people do well with, but if we don't figure out how being pre-disposed to having issues with LDL receptors really changes things, we are going to (deservedly) get hammered by the low-fat whole grain camp when a fair amount of people who thought they had it all figured out are dropping dead from eating fats because they are ApoE and had no idea.

    I'm genuinely glad that my example is helping people. No doubt I am. But I'd be alright with feeling like I'm getting somewhere with all this in my personal case as well. At the moment, I can't really say that I feel that way just yet.

  • Dr. K

    8/11/2011 12:38:34 AM |

    Patients with apoe4 have a higher rate of AD and AD is associated with a cholesterol deficiency in the brain.  So for me apoe4 is a signal to load with the MCT of coconut oil which has massive benefits to the brain metabolically.  I find it hard to believe this is bad for the heart at any level because CAD tends to mirror CVD across all measures.  I think only cardiologist have this problem with Larger particle LDL because of the faulty lipid hypothesis.  cAD is an inflammatory condition.  It ha little to do with cholesterol itself.  If the cholesterol is oxidized then there are issues but this can be followed by acute phase reactants from the liver like HS CRP.  When it's up HDL tends to be low......and it's low because the liver is being bombard by gut endotoxins and this is a direct measure of the oxidation potential of an overwhelmed portal circulation.  To further the point......thyroid hormone, testosterone, estrogen, and high vitamin D levels all raise liver HDL and this is how they protect against heart disease.  I maintain large LDL confers no risk without inflammation.......and a low HDL is a great way to know if your liver is being overwhelmed in the portal circulation.  This is why vitamin K2 confers a great cardiac benefit.......it comes from a healthy gut biome.  vAP tells you a ton about your portal circulations inflammatory burden.

  • majkinetor

    8/14/2011 2:59:37 PM |

    M-Al, just copy your text prior to the post, or write it in the editor. I don't know which browser you use, but in Chrome if you use "back" on "server error", it will return what you typed in a reply.

  • Peter Silverman

    8/16/2011 5:08:49 PM |

    Following your diet I took an NMR last summer and this summer.  The small LDL particles went down (835 to 709) but the total particles went up (1800 to 2100).  Should I stick with your diet (low carb, no wheat, D, omega3's), one Walmart glucometer) or go back to rice and beans?

  • Jack Kronk

    8/24/2011 7:29:11 PM |

    I got quote at $390 for just an ApoE genetic test. Is that normal?

  • Adriana

    10/5/2011 12:33:30 PM |

    Have you seen any reduction in your LDL following this diet?

  • Eric

    7/9/2012 6:43:01 PM |

    I've been eating paleo/primal for about a year, dropped 10 pounds, and brought my triglycerides down from a high of 325 three years ago to 130. Unfortunately, my LDL-p is over 2600 (first time it was checked), and I found out I'm APO e4/e4.

    The doctor says e4/e4 should go vegan, which seems about as anti-primal as you can get.

    Any suggestions for where to start looking for eating guidelines?

  • Gary Mullennix

    5/4/2013 4:38:16 AM |

    My goodness, how very confusing!!  I'm hypothyroid.  My HDL is 95. My total C is 285. Ny LDL is 186. But my LDL fractions are mostly big and plumb and my small total 23. So, I think I'm ok...buy my doc thinks I should go vegan. I want coconut oil, little red meat.  I evercise 5x week. My heatt stress tests were all 'well within'   So, it sounds as though I need to get the E4 tested   More?

  • Mario

    3/9/2014 9:46:46 AM |

    I would be deeply grateful for your advice. I am doing my best to understand how to cope with my aPOE 3/4 status. I have Alzheimer's on both sides of my family, which has killed or is in the process of killing several relatives, including my father and maternal grandmother. Unsurprisingly, I have received much conflicting data.

    I am 46. I eat a strict Paleo diet (grass-fed, wild-caught, etc.) except for some resistant starch in the form of parboiled rice and unmodified potato starch. I consume approximately 50-60% fats (majority saturated fats including daily MCT oil), 30-40% protein and 10-20% carbs. I exercise vigorously and non-vigorously -- but not every day. (Incidentally, over three years I naturally increased my testosterone by 38% using this approach, going from the low 3's to 5.3.)

    My LDL is 128. My HDL is a distressingly low 33. Triglycerides are 59.

    MY NEXT MOVE: Seek out an LDL particle-size test. If that reveals my LDL particles to be of an unhealthy size then I will need to consider a different approach in regard to sat fats. Also, looking  to improve my sleep, which has been my Achilles' heel (consistently get only around six hours). Finally, using super-consistent exercise and increasing oyster intake to boost the HDL.

    I would appreciate any guidance.(!)

    Best / Mario

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