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Creamy Cauliflower Sauce

from http://pinchofyum.com/creamy-cauliflower-sauce

March 18, 2013

This. Sauce. I make it all the time. I use it in tons of recipes. I spoon-feed it to myself straight out of the blender.
So it’s only appropriate that I dedicate an entire post to my all-time favorite, super adaptable, absolutely totally delicious creamy cauliflower sauce. The garlic, butter, creamy cauliflower cooked to perfection all pureed up in that blender (or food processor, because you have a well stocked kitchen unlike me even though I blog about food, say what?) is just life changing.
I honestly have a hard time NOT putting it in every recipe that I make. If something seems to be lacking, this sauce just magically pops into my mind. Bing! Like, hey! maybe a little cauliflower sauce will help this recipe be amazing! Which is a great idea until things start to get out of control as is often the case in my brain, and somehow I find myself wondering if cauliflower sauce would be good in pumpkin bread. Gross. No, it wouldn’t. But maybe…
Too much, Lindsay. Too much.


This sauce is really flexible. It can kinda become anything.
Mostly for me, it becomes Alfredo sauce for my noodles and I call it Healthy Fettuccine Alfredo.

And it can also become creamy cauliflower garlic rice. Good grief, I love this stuff.

Hey guess what? Coming soon it will become sauce for a white pizza. Yeahhhh there’s a reason why I want you to have this recipe in your head. A reason that involves thick yummy whole wheat crust, this sauce, white melty cheese, chicken, tomatoes, and on, and on, and on, and on.

Before I launch you into the recipe, I feel like I should say this: this is not made from cream and butter and flour. It’s made from caul-i-flower. Get it? Flour? Flower? While I personally consider this sauce to be magical, it’s not going to taste like it’s made from cream and butter. Well, actually, it kind of does, and MANY of you have said how much your cauliflower-hating families loved this sauce, so who knows. I just want to remind the skeptics that this is indeed cauliflower sauce, so you can expect it to be at least a little bit, um, cauliflowery.
And creamily delicious.
Did I already mention howmuchIlovethisstuff?

4.9 from 13 reviews

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Creamy Cauliflower Sauce

Author: Pinch of Yum

Serves: makes about 5 cups

 

Ingredients

• 8 large cloves garlic, minced
• 2 tablespoons butter
• 5-6 cups cauliflower florets
• 6-7 cups vegetable broth or water
• 1 teaspoon salt (more to taste)
• ½ teaspoon pepper (more to taste)
• ½ cup milk (more to taste)

Instructions

1. Garlic: Saute the minced garlic with the butter in a large nonstick skillet over low heat. Cook for several minutes or until the garlic is soft and fragrant but not browned (browned or burnt garlic will taste bitter). Remove from heat and set aside.
2. Cauliflower: Bring the water or vegetable broth to a boil in a large pot. Add the cauliflower and cook, covered, for 7-10 minutes or until cauliflower is fork tender. Do not drain.
3. Puree: Use a slotted spoon to transfer the cauliflower pieces to the blender. Add 1 cup vegetable broth or cooking liquid, sauteed garlic/butter, salt, pepper, and milk. Blend or puree for several minutes until the sauce is very smooth, adding more broth or milk depending on how thick you want the sauce. You may have to do this in batches depending on the size of your blender. Serve hot! If the sauce starts to look dry, add a few drops of water, milk, or olive oil.

Notes

I like to add a little bit of olive oil for the flavor and to help keep the sauce really smooth. Several other readers have mentioned that they really liked the addition of Parmesan cheese as well.

**Serving size is 1/2 cup.

http://pinterest.com/julibauer/paleomg-recipes/

Primal Biscuits

The one on the left I sprinkled with cinnamon before I baked it then spread it with almond butter and coconut flakes, ssssssmart!


(WOW!  WHEN I PULLED UP THIS RECIPE, SHE USED THE F BOMB IN HER COMMENTS BEFORE GIVING THE RECIPE.  I WAS SO STUNNED BY THAT.  SO I DON'T FEEL COMFORTABLE POSTING THE LINK ON THE BLOG LIST BUT I THINK HER RECIPES MAY HAVE MERIT.  WON'T THROW THE BABY OUT WITH THE BATH WATER.  

INGREDIENTS:

• 1/2 cup almond flour.
• 1/4 cup coconut flour.
• 1/4 cup flax meal.
• 1 tbsp melted ghee.
• 1/4 cup coconut milk.
• 1 tsp baking soda.
• 1/2 tsp salt.
• 6 egg whites (don't throw away the yolks, save them for Paleo Mayo, shakes, or scramble them up and eat them like a champion.)

PROCESS:

1. Combine the dry ingredients into a bowl while your oven heats up to 350.
2. Combine the ghee, coconut milk and egg whites in a blender until frothy.
3. Incorporate the wet and dry and add seasonings of choice (I poured mine into the muffin tins then topped with seasonings so I could make 3 different kinds.)
4. Grease 6 muffin tins, 3 larger ones with coconut oil and scoop your batter in filling them halfway.
5. Bake at 350 degrees for about 18 min (large biscuits, 15 for small), keep an eye on em. 

http://www.thefoodee.com/recipe_authors/3086/

Juli's Cookbook

Pumpkin Cashew Coconut Curry over Coconut Rice

by Juli

Prep time:  10 mins

Cook time:  15 mins

Total time:  25 mins

Serves: 4-5

 

Ingredients

For the curry

• 1lb chicken, cut into cubes
• 2 garlic cloves, minced
• 1 red onion, sliced
• ⅔ cup canned coconut milk
• ½ cup pureed pumpkin
• ½ cup cashews
• 2-3 tablespoon curry powder
• 1 tablespoon Gold Label Virgin Coconut Oil
• 1 teaspoon ground cumin
• ½ teaspoon cayenne pepper
• ¼ teaspoon red pepper flakes
• pinch of cinnamon
• salt and pepper, to taste
• cilantro, to garnish

For the coconut rice

• 1 head cauliflower, stem removed, roughly chopped
• ⅓ cup canned coconut milk
• ¼ cup Unsweetended Shredded Coconut
• 1 tablespoon Gold Label Virgin Coconut Oil
• 1 teaspoon raw honey
• pinch of salt

Instructions

1. First add your chopped cauliflower to your food processor with the shredding attachment to “rice” the cauliflower.
2. Pull a large pot, place over medium heat, and add a tablespoon of coconut oil then add your cauliflower. Add a pinch of salt, then cover to help steam, mixing occasionally.
3. Now pull out a large skillet and place under medium heat. Then add your coconut oil.
4. Add minced garlic then chicken as soon as the garlic becomes fragrant.
5. Once the chicken begins to become white on all sides, add your ⅔ cup coconut milk and pureed pumpkin to your chicken and mix until the pumpkin breaks down.
6. Now add your sliced onions and spices to cook down.
7. Then add your other ingredients for your coconut rice and cover to cook down. Stir occasionally to make sure it doesn’t burn!
8. Let the rice cook for about 5-8 minutes until coconut milk has evaporated and you have sticky rice.
9. When chicken is done cooking and your curry has thickened a bit, remove from heat and add your cashews to the curry mixture.
10. Now place sticky rice in a bowl along with curry over top and cilantro to garnish!

Coconut Flour Conversion Guide

Coconut flour conversion

Here is a chart to help when converting to coconut flour from other flours. 

Client Testimony

Another client's testimony on cholesterol and blood sugar... I just LOVE getting these!

Working with Maria was the BEST thing I have done! It was worth every dime I spent …. and I am ever so grateful for her! When I began working with Maria, it was 4-5 months after I had a heart attack. My weight during that time was 182 lbs on my 5 foot 6 inch frame. I had type 2 diabetes and also an A1c that was 8.3 (way out of the normal range.) Total Cholesterol 257, Triglycerides 158, LDL 183, HDL 42. 

On the insisting of my daughter, I signed up to work with Maria. I followed her plan and her recipes and supplements she suggested for me. I was amazed at how accurate her suggestions were later after consulting an Integrative Cardiologist, who has continued to help with the recovery of my heart function. Following Maria's advice was the best step I have had in the turn around of my health. 

Within 3 months of her plan, my weight had dropped to 163, and I astounded my doctors not only with weight loss, but my blood work too. My A1c dropped down to 6.4, then 5.5 on the next reading. Cholesterol levels were lowered, my blood sugar readings were lower…and I felt better than I had in years! 

After a few months of her plan my Cholesterol Total was 166, Triglycerides 75, LDL 96, and HDL 55. Today, now 1 year and 7 months later after starting with Maria, I am now down to 153 lbs (Triglycerides dropped to 54!) and continue to feel great! My A1c and cholesterol levels are all within normal range and I truly owe my gratitude to Maria for all her hard work. Not to mention, her recipes are delicious too!! THANK YOU MARIA!!! 

Annette M.

Good Fats, Bad Fats and What Causes Cholesterol

from MariasHealth

Cholesterol Part 3 - How Can We Reduce Our Risk?

Friday, April 26, 2013

In this third and last post on cholesterol and Coronary Artery Disease (CAD) we will talk about what you can do to lower your risk.  In the first post we broke down the myths of the Lipid Hypothesis (located HERE) and in the second we covered what really causes Coronary Artery Disease (CAD) (located Here).

As I eluded to in the first post, CAD is primarily caused by oxidative damage and inflammation.  The 4 primary causes of oxidative damage and inflammation are:

1. Poor Nutrition
2. Stress
3. Smoking
4. Physical Inactivity

Let's break each these factors down.

Smoking

So we all know we shouldn't smoke.  Smoking as few as 1-4 cigarettes a day increases your CAD risk by 40%.  40 a day increases risk by 900%!!   I don't think I need to say much more on that one.

Physical Inactivity

We also know that being physically active is important.  People that are not physically active have 1.5x to 2.4x the risk for heart disease.  Currently more than 60% of Americans are not regularly active and 25% are completely sendentary.  Regular excessive reduced both inflammation and oxidative damage.  There are many ways to increase your physical activity.  It doesn't mean you have to go to them gym and run on a treadmill.  Just going to the grocery store, parking at the far end of the lot, shopping for your food and coming home to cook a meal instead of going through the drive through can make a difference.  Walk around the block and increase from there.  Walk the dog.  There are a lot of activities that we can do to increase our excessive and reduce our risk of heart disease.

Stress

Stress is important to keep low as this can be a big contributor to CAD risk.  This Study showed that stress can triple the risk of heart disease.  This is when we get that "fight-or-flight" response that we experience when under high stress.  This elevates cortisol which causes both oxidative damage and inflammation. A great way to reduce stress and increase physical activity is with something like Yoga!

Poor Nutrition

The best thing you can do to influence your risk of CAD is through diet.  This study of 52 countries found that 90% of heart attacks could have been prevented through diet.  That's right, 9 out of 10 heart attacks could be prevented without drugs.  So what foods cause oxidative damage and inflammation?  There are several sources and we will break down the biggest ones.  This biggest contributors to oxidative damage and inflammation are sugar (sucrose, fructose, etc), starch (grains, etc), polyunsaturated (PUFA) oils and trans fatty acids (transfat).

Sugar!

One of the best studies on sugar consumption and how it relates to cholesterol levels is the 2011 study by Peter Havel and colleagues titled Consumption of fructose and HFCS increases postprandial triglycerides, LDL-C, and apoB in young men and women.  In this study they had 3 groups in a randomized trail and had them consume the Standard American Diet (SAD) (55% carbs, 15% protein, 30% fat) with the difference being where the carbs came from in each group.

Group 1: 25% of their total energy from glucose (so traditional sources, sort of the SAD control group)
Group 2: 25% of their total energy from fructose
Group 3: 25% of their total energy from High Fructose Corn Syrup (HFCS) (55% fructose and 45% glucose)

This 25% of their diet coming from sugar equals about 120 pounds of sugar per year.  That may sound like a lot, but that is actually below the current average for Americans.  This figure shows the differences in LDL-C, non-HDL-C, apoB, and apoB/apoA-I.

This is a very powerful indication that while glucose and fructose alone can be bad in excess, their combination seems even worse.  It would have been really interesting to have an additional group that removed most carbs all together.  (more on this in the carb section below)

Sugar and fructose are very inflammatory and cause lots of oxidative damage.  What happens is when we consume large amounts of sugar and fructose, our insulin levels go up and it is this rise in insulin that causes tears in the artery wall.  Cholesterol comes to repair this oxidative damage and build up causing plaque build up (as described Here in part 2).  So it is imperative to keep our blood sugar levels (and thus insulin levels) balanced so that we don't cause this inflammation and oxidative damage.  So keeping sugar and starch low in our diets (to keep our blood sugars balanced) becomes the best way we can change our diet to reduce our chances of getting CAD.

Also important to note, as I did in This post, non-alcoholic fatty liver disease and metabolic syndrome are very big factors in CAD risk (as much as 14 times in women).  So what causes non-alcoholic fatty liver disease?  There is growing evidence that fructose consumption (fruits, fruit juices, etc) are a big contributor as well as high fructose corn syrup (source and source).  When you consume fructose 100% of the metobolic burden rests on your liver.  Only your liver can break it down.  Glucose is only 20% broken down by the liver and the remaining 80% is immediately metabolized and used by the cells in your body.  When fructose is converted into fat, it gets stored in your liver and other tissues as body fat.  120 calories of fructose is stored as 40 calories of fat in your body.  120 calories of glucose gets stored as less than 1 calorie in your fat stores. Fructose metabolism is very similar to alcohol making it one of the biggest contributors to non-alcoholic fatty liver disease.

Fructose also worsens insulin resistance which speed metabolic syndrome.  This is a good video with more info on sugar.

Carbs

There is a great study by Jeff Volek that looks at the results of a carbohydrate restricted, high fat diet compared to a low fat high carb diet and the results on cholesterol (source).

The two groups in the study were taken from a SAD diet to a carb-restricted diet (CRD or Very Low Carb, High fat diet) and low-fat diet (LFD or Very Low Fat, High Carb diet).  As you can see the high fat diet was mostly fat (100g or 900 calories) and very little carbs (44g or 176 calories).  Here are the results after 12 weeks on each diet.

As you can see the Low Carb/High Fat diet reduced Triglycerides significantly and also reduced insulin levels greatly.  The Low Fat diet had statistically insignificant changes in both triglycerides and insulin levels.  As we discussed in the last post, LDL particle number is the best predictor of CAD risk, but other measurements like Triglycerides can be indicative of issues that can contribute to high LDL-P.  It is good to keep your fasting Triglycerides below 88.  

Good Fats

This is the component you want to increase the most (while decreasing carbohydrates) to help protect against heart disease.  Especially important are saturated fatty acids (SFAs).  Saturated fats like coconut oil, butter, ghee, tallow and lard are protective against oxidation and inflammation and have many other important health benefits.  I will have a post on fats coming soon to expand on this topic in greater detail. Studies like This one published in the Journal of Nutrition 2004 showed that saturated fat from MCT oil (medium-chain fats similar to those in coconut oil) and beef tallow reduced alcohol-induced liver damage when substituted for polyunsaturated corn oil. In fact, they replaced 20 percent, 45 percent, or two-thirds of the corn oil with saturated fat and found that the more saturated fat they used, the greater the protective effect.  So saturated fat can be protective against one of this biggest risk factors for CAD, fatty liver disease.  Here is another recent study showing the protective affects of coconut oil.  There are several good oils that can be very helpful in reducing your CAD risk.  Also, the higher the saturated fat content the better.  Here are the best oils:

1. Coconut oil: 1.9% (92% saturated fatty acids (SFA))
2. Cocoa Butter: 3% (with 60% SFA)
3. Beef Tallow: 3.1% (with 49.8% SFA)
4. Ghee: 4% (with 48% SFA)
5. Butter: 3.4% (with 50% SFA)
6. Macadamia oil: 10% (with 15% SFA)
7. Avocado oil: 10% (with 11% SFAt)
8. Lard: 12% (with 41% SFA)
9. Duck fat: 13% Omega-6 PUFA (with 25% SFA)
10. Almond oil: 17% (with 8.2% SFA)

So we should be consuming lots of these oils in order to reduce our CAD risk (as well as a huge number of other health benefits).

Bad Fats

There are two kinds of fats that should be avoided.  The most inflammatory fat is Trans Fatty Acids (transfat). Transfats are one of the worst substances we can consume for our overall health.  There are many studies that show the heart disease and cancer risks of transfat (source, source, and many more for cancer, source and source).  Even the FDA has stated that "Further reducing trans fat consumption by avoiding artificial trans fat could prevent 10,000-20,000 heart attacks and 3,000-7,000 coronary heart disease deaths each year in the U.S." Here is a list of transfats to avoid:

• Margarine
• Vegetable Shortening
• Ingredients that list Hydrogenated (fully or partially) Oils

Poly Unsaturated Fatty Acids (PUFA's) are also bad oils as they are easily oxidated.  This means they are very susceptible to oxidative damage, the thing that increases our CAD risk.  There are many PUFA oils and here is a short list:

• Grapeseed oil: 70.6% Omega-6 PUFA
• Sunflower oil: 68%
• Flax oil: 66%
• Safflower oil: 65%
• Corn oil: 54.6%
• Walnut oil: 53.9%
• Cottonseed oil: 52.4%
• Vegetable oil (soybean oil): 51.4%
• Sesame oil: 42%
• Peanut oil: 33.4%
• Canola oil: 19%
• Olive oil: 9.9% (with 14% saturated fat) (although this one is ok in moderation, and never for cooking which will cause oxidation.  So only use in dressings, etc.) 

What has happened over the last 100 years is a huge increase in PUFA consumption and a reduction in other good fats (like saturated fat).  Here is a chart showing the increase in PUFA consumption in the US.

It is my belief that this is a huge contributor to our increase in heart disease.  So it is imperative to reverse this trend if we want to reduce the incidence of heart disease.

Summary

There are many things you can do to reduce your risk of coronary artery disease (CAD).  Some of these are obvious (quit smoking, reduce stress, increase physical activity).  But nutrition can be the largest factor (preventing as much as 90% of heart attacks).  The biggest nutritional contributor to CAD risk is sugar.  High fructose corn syrup and fructose are particularly bad but all sugars will contribute and should be eliminated as much as possible.  Other starchy foods also contribute to oxidative damage and inflammation so keep starchy food consumption as low as possible also helps CAD risk.  Lastly, the good fats (saturated fats, coconut oil, MCT oil, ghee, butter, tallow and cocoa butter) are very protective against oxidative damage and inflammation and should be consumed in high quantities in order to reduce your risk of CAD.  The bad fats are the transfats and PUFA's and should be avoided.  So eating lots of good fats, moderate amounts of protein and very low carbs (especially sugars) are the best ways to reduce your CAD risk.  In addition supplementin with CoQ10 can help decrease oxidation and improve heart health.

Cholesterol Part 2 - What Causes Coronary Artery Disease (CAD)

Friday, April 19, 2013

In the first post (located Here) we talked about the myths about Cholesterol.  In this post I am going to do my best to take a very complex issue (something I guarantee about 95% or more of Doctors don't know) and explain it in an easy to understand way. Lets take a look at how Cholesterol is transported through the body and what causes Coronary Artery Disease (CAD).  In the final post on cholesterol we will talk about what you can do to reduce your chances of getting CAD.

How is Cholesterol Transported?

Cholesterol (lipids) needs to get from point A to point B in our bodies.  There are two types of substances that travel through our blood stream.  Hydrophilic and Hydrophobic.  Hydrophilic substances can travel in the blood without assistance because it is not repelled by liquid (like salt or sugar which dissolves in water).  Hydrophobic substances need a transporter in order to travel in the blood because they are repelled by liquid (like oil which is repelled by water). Cholesterol is hydrophobic which means to travel around the body it needs a carrier. That carrier is a protein molecule called apoproteins. Once they are bound with cholesterol they are called apolipoproteins (apo).  There are two main classes of apo's, apolipoprotein A-I (apoA-I) and apolipoprotein B (apoB).  Almost all apoB in our body is found in low-density lipoprotein (LDL), while most apoA-I in our body is found on high-density lipoprotein (HDL).

But this all deals with the surface of the lipoprotein molecule.  If you think of this molecule as a ship, this is all dealing with the surface of the ship.  But what about the cargo?  Remember, these ships are serving as cargo carriers for the cholesterol lipids (both on the surface and inside).  Something that is important is the ratio of lipid-to-protein which determines its density.  Something with high density is heavier for a given volume than something of low density.  A cubic inch of Lead will weight much more than a cubic inch of Styrofoam.  Remember this chart from part 1 on cholesterol?

This chart shows the rough breakdown of the different cholesterol particles.  Another way to look at this breakdown is based on the following groupings.  There are five main classes:

1. high density lipoprotein (HDL)
2. low density lipoprotein (LDL)
3. intermediate density lipoprotein (IDL)
4. very low density lipoprotein (VLDL)
5. chylomicron

Now look at this table:

This table shows the relative density of these five groups.  Notice the very small difference in density between the most and lease dense lipoprotein.  But, also notice the very large difference in diameter (as much as 100 times). The below chart gives us a more visual look at all the different lipoproteins and their composition.

Source: Lecture by Tom Dayspring (source pdf)

Note that ApoA lipoproteins (HDL) are tiny compared to ApoB lipoproteins (VLDL, IDL and LDL).  This figure is not to scale so the difference in size is actually much greater than shown.  As you move in size from larger to smaller, the amount of triglycerides (TG) goes down and protein goes up (in relation to the total volume).  

Cholesterol transportation goes both ways.  It travels from the gut and liver to our cells (muscles and fat cells for energy, cell repair, etc).  It also travels back to the liver, primarily from LDL.  So most of the cleaning up of cholesterol (returning it to the liver) is done by the supposed "bad" cholesterol (LDL).  The problem is, sometimes LDL can penetrate and deliver it's cholesterol to our artery walls.  This is what we don't want to have happen.  It is the ApoB particle that drives the cholesterol into the artery wall and 90-95% of ApoB particles are LDL.  

Coronary Heart Disease (CAD)

The basic process is the LDL particle (LDL-P) crashes into the artery wall and delivers it's cholesterol.  This stimulates an inflammatory response and our immune system kicks in and tries to fix this inflammation by removing the cholesterol from the artery wall. This immune response actually creates a space for more LDL-P to be retained.  Sort of like cement holding them in.  More and more LDL-P enter the space being created by the immune response.  Eventually, through more retention of LDL-P and advanced immune response, not only does the artery narrow, but a cap of tissue forms which is known as plaque.  Most heart attacks occur when a piece of this plaque breaks off and blocks blood flow.  

So what causes the LDL-P to attach to the artery wall?  The main reason is when there is damage or inflammation. This inflammation is primarily due to oxidative damage or oxidation.  This oxidation could be in the artery wall (lesion), causing an immune response and thus the build up of white blood cells and LDL particles in the cavity that is created.  There can also be oxidation of the LDL particle itself.  Studies have shown that oxidated LDL cholesterol is 8 times stronger a risk factor for CAD than normal LDL.  

There are also some important things to know about LDL particles.  Small dense LDL particles are more likely to become oxidize than large fluffy LDL particles.  Small dense LDL particles are more likely to fit into the lesions in the artery wall (vs. large fluffy).  One of the problems though is that particle size tests are not standardized and can vary from one test type to the next.  Also, there aren't good ways to measure oxidized LDL.  This makes testing somewhat varied.  Also, particle size is a secondary factor in that it is only important if your LDL-P is high (more on that below).

So oxidation and inflammation is the major concern with dealing with CAD.  What are the 4 primary causes of inflammation and oxidation?

1. Smoking
2. Poor Nutrition
3. Physical Inactivity
4. Stress

We will break down in our next post how we can reduce these causes of oxidation and inflammation.

A Couple Notes about Testing and Variability in Levels:

In one person, studies have shown that with no change in diet or lifestyle, the total cholesterol can vary by about 35 points up or down for no reason at all.  HDL can vary up or down about 9 points.  LDL by 30 points.  The ratio of Total/HDL up or down by 0.8.  Triglycerides (TG) about 40 points.  This means a couple things.  You need to see fairly large changes in your numbers to conclude that something has changed.  Second, a single test doesn't give you the whole picture.  You need several tests to see what your average level is.  So you could get tested today and have a total cholesterol of 200 and go back in tomorrow and have a level of 235 (or 165) and that is a totally normal variation.

Another important point is that when you are losing weight, your cholesterol levels will be skewed until you settle at a new body weight (cholesterol release into blood from fat cells).  So testing cholesterol right after losing significant weight will show higher levels until your weight has settled.

Another example is when you have non-alcoholic fatty liver disease and you change your diet to correct this, the lipids and cholesterol stuck in the liver will be release into the bloodstream and thus raising your TG and LDL numbers.  But this is a good thing as your liver is release them to heal and over time the levels will go back down.

Another note is that in a Japanese study (source) they showed that non-alcoholic fatty liver disease can be a really big indicator of risk for Coronary Artery Disease (CAD).  Non-alcoholic fatty liver disease increased the risk of CAD by 3 to 4 times for men and about 14 times for women.  So there are some scientist that now believe that non-alcoholic fatty liver disease may be one of biggest indicators of future CAD risk.

How to Determine your CAD risk

What the latest science has shown is that ApoB or LDL particle (LDL-P) is the best indicators of metabolic syndrome (and thus CAD risk).  So what is important is the number of LDL particles not the amount of cholesterol contained in them (LDL-C).  (source)

It is sort of a probability game.  The more LDL particles there are, the higher the chance they will crash into the artery wall and deliver their cholesterol.  The LDL particle number (LDL-P or ApoB) is the best predictor of risk for CAD. Some statements have been made about the size of the LDL particles as being an important factor in determining your risk for CAD (small dense particles due to oxidation are bad, large fluffy good), but the latest science (within the last couple years) shows that this is a secondary factor.  The LDL-P number is more important and only when LDL-P is high does the size become important.  Take a look at this graph from Quebec Cardiovascular Study, published in 1997, in Circulation.

Graph from Quebec Cardiovascular Study, published in 1997, in Circulation (Source)

What this graph shows is that for patients with low LPL-P (below 120) the size of the LDL particles does not matter (same risk of 1.0).  But for those with High LDL-P (above 120) the size becomes very important (Those with larger particles only had a 2X risk versus a 6.2X risk for those with the smaller particles).

There are several methods for measuring cholesterol, but I will not go into detail about the all of them (THIS source does it much better than I would).  However, let's look at the one test that is the most important.  The best measurement and only one that actually directly counts the LDL-P is nuclear magnetic resonance spectroscopy or NMR for short (called NMR LipoProfile).  Here is what an NMR report looks like. 

Source Here

This test counts the total LDL particles (LDL-P), HDL particles (HDL-P), apoB and apoA-I.  It also measures the size of each particle.  The particle size is very telling when it comes to predicting insulin resistance (and Metabolic Syndrome).  In the results below you can see that this person has small VLDL particles and small HDL particles.  When there are large VLDL-P, large VLDL size, increased small LDL-P, small LDL size, reduced large HDL-P, small HDL size are markers for insulin resistance.  These findings can precede more conventional signs for insulin resistance in many cases by several years. 

Source Here

What is important to note here is that the traditional LDL cholesterol (LDL-C) of traditional tests given by most doctors today isn't the same as LDL particles (LDL-P) and doesn't necessarily correlate to LDL-P.  In other words if your LDL-C is low, your LDL-P could still be high (more particles which are smaller and contain less cholesterol).  This is particularly true for those with metabolic syndrome and diabetes. (below is from HERE with my own text to help easier understanding of this complex issue)

Patients with LDL-C between 100 and 118 mg/dL are shown without metabolic syndrome (top) and with metabolic syndrome (bottom). In the patients without metabolic syndrome, LDL-C under-predicts cardiac risk 22% of the time. However, when you look at the patients with metabolic syndrome, you can see that 63% of the time their risk of cardiac disease is under-predicted.

The above data was collected from nearly 2,000 patients with diabetes who presented with “perfect” standard cholesterol numbers: LDL-C less than 70 mg/dL; HDL-C greater than 40 mg/dL; TG less than 150 mg/dL.  But only 22% of the time did the LDL-P (the real indicator of risk) equal the LDL-C levels.  Remember that LDL-C less than 70 mg/dL is considered VERY low risk (5th percentile).  But with LDL-P the real risk for 35% of these patients was above 1000 nmol/L (above 20%) and 7% were HIGH RISK.  When you do this analysis with less stringent LDL-C criteria (LDL-C less than 100 mg/dL) the number of patients in the high risk group is even higher.  This shows that for many people with metabolic syndrome or diabetes, the LDL-C numbers inaccurately report their real risk for CAD.

Summary:

To summarize this very complex issue, LDL particle number (LDL-P) is a great indicator of Metabolic syndrome and is the most accurate predictor of CAD risk, not the traditionally used LDL-C. The best test for LDL-P is NMR LipoProfile.  There are many other markers that can give you information about what is going on in the body (Triglycerides, Ratio of Total cholesterol to HDL, Total HDL levels, etc.) but none of them on their own accurately predict the risk of CAD except LDL-P.  Also, non-alcoholic fatty liver disease is a very good predictor of future CAD.  

So if you have received an NMR LipoProfile and have found that your LDL-P is high or just want to ensure it doesn't get to a dangerous level, what do you do about it?  In the next post we will talk about how to reduce your LDL-P and your risk of coronary artery disease.

The Cholesterol Myth

Friday, April 12, 2013

The Cholesterol Myth

This post is by Craig, Maria's husband.  I am a science geek but like to research and put things in easy to understand format.  In this post (and the next one) I will break down the whole issues of cholesterol.  There is a hypothesis that says eating food high in cholesterol and saturated fat causes high cholesterol in your blood which causes coronary artery disease (CAD). It's called the Lipid Hypothesis. This is what the majority of Doctors and Cardiologists believe. So lets break it down piece by piece and expose the myths that lie in every leg of the Lipid Hypothesis.

What is Cholesterol

First, lets talk about Cholesterol and what it's purpose is in our bodies. Cholesterol is our bodies main repair mechanism. It comes into action whenever there is inflammation to repair that inflammation. Saying you need to lower cholesterol is killing the messenger. It's like killing half the firefighters that come to put out a fire. It won't help put out the fire or what caused the fire, it will make it harder.

There are two main forms of cholesterol. Low-Density Lipoprotein (LDL) and High-Density Lipoprotein (HDL). In the Lipid Hypothesis it is generally thought that HDL is the good cholesterol and LDL is the bad cholesterol. The general theory is that if your total cholesterol is above 200, you are in danger and need to go on a statin drug to lower your cholesterol (more on that later). But the total cholesterol is HDL+LDL. So too much of a good thing (HDL) can lead to a bad thing (too high total cholesterol)? This is the first of many contradictions of the Lipid Hypothesis. If you start digging into the science, it get even more confusing.  Recent studies have shown that there is Bad Bad cholesterol (small dense LDL), Good Bad cholesterol (large fluffy LDL) and intermediate LDL (which can be good or bad depending on when they occur). Then there is Good Good cholesterol (HDLs 1 &2) and Bad Good cholesterol (HDL 3). Now the Total Cholesterol number looks even more convoluted.

Saturated fats and cholesterol make the membranes of the cells firm—without them the cells would become flabby and fluid. Cholesterol and saturated fat act as the conduits enabling all of the cells in our body to communicate. Cholesterol and stiff saturated fatty acids form "lipid rafts", which make little parking spots for every protein in the membrane and enabling it to perform its functions. Without cholesterol and saturated fats, our cells would not be able to communicate with each other or to transport various molecules into and out of the cell. As a result, our bodies would not be able to function the way they do. The human brain is particularly rich in cholesterol: around 25 percent of all body cholesterol is accounted for by the brain. Every cell and every structure in the brain and the rest of our nervous system needs cholesterol, not only to build itself but also to accomplish its many functions. (source)

One of the most abundant materials in the brain and our entire nervous system is a fatty substance called myelin.  Myelin coats every nerve cell like the coating on electric wires.  It provides nourishment and protection for our brain and nervous system.  People who lose this protective coating develop a condition called multiple sclerosis (MS).  Myelin is composed of over 20% cholesterol.

Many of the hormones in our body are made from cholesterol (testosterone, progesterone, pregnenolone, androsterone, estrone, estradiol, corticosterone, aldosterone and others). In our stressful modern lives we consume a lot of these hormones which can lead to Adrenal Fatigue.  In addition  every sex hormone in our bodies is made form cholesterol.  So without it, we wouldn't be able to have children.

Our livers make bile out of cholesterol, so even digestion and our ability to absorb fats and fat-soluble vitamins is dependent on cholesterol. Cholesterol also plays a vital role in our immune health.  And most importantly (back to our original point), the liver sends cholesterol to the site of an injury or inflammation.  This is one of cholesterol's most vital roles. Cholesterol and fats are essential in removing toxins and healing. This is why blood cholesterol levels go high after a surgical procedure.  The liver is sending out lots of LDL cholesterol to clean and heal the cuts and damage from the surgery. LDL also goes up when dealing with an infection, bacteria or viral attack.

Blood cholesterol levels of between 200 and 240 mg/dl are actually quite normal. In older women, serum cholesterol levels greatly above these numbers are also quite normal, and in fact they have been shown to be associated with longevity. In this study it is shown that the higher the number, the less mortality by all causes, heart disease, cancer, etc.

So as you can see cholesterol and saturated fat are vital to our bodies and our health. We wouldn't be able to live without them.

Myth 1: Eating Cholesterol and Saturated Fat leads to High Cholesterol

This is actually pretty easy to dispel.  The longest running study and perhaps most significant study on heart disease is the Framingham Heart Study (followed 15,000 participants over 3 generations).  It has shown that dietary intake of cholesterol has absolutely no correlation to heart disease.  This chart shows the results and as you can see there are nearly identical rates of heart disease among men and women regardless of their cholesterol intake (above or below average).

The Framingham study also found the same to be true about saturated fat intake:

"In Framingham, Mass., the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol. The opposite of what… Keys et al would predict"

Even Ancel Keys, the father of the Lipid Hypothesis said in 1997:

"There’s no connection whatsoever between the cholesterol in food and cholesterol in the blood. And we've known that all along."

Gary Taubes wrote a great piece on why this became the "law of the land" and the politics behind it (source).

Myth 2: High Cholesterol causes Coronary Artery Disease (CAD)

So this is where we are killing the messenger.  Yes, high cholesterol is present, but it is not causing the problem, it is there to fix the problem (inflammation, more on that in our next post).   There are numerous studies that dispel this myth.  First, there is no correlation by country.  Here is a video that shows how countries with the highest cholesterol levels (like Switzerland) have low heart disease rates and people like the Australian Aboriginals who have one of the highest rates of heart disease also have one of the lowest blood cholesterol levels.

Another example is the Conference on Low Blood Cholesterol which reviewed 11 major studies including  125,000 women and determined that there was absolutely no relationship between total cholesterol levels and mortality rate from cardiovascular or any other causes (source).

There are also more than 40 trials (source) performed to determine whether lowering cholesterol levels can prevent heart disease.  In some trials the rates went up, others they went down.  But on average, when all taken together, just as many people died in the groups taking cholesterol lower drugs as those with no treatment.

Lastly and possibly most alarming is that there is evidence that points to lower cholesterol leading to higher death rates. Again form the Framingham Heart Study:

“There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years.”

So as cholesterol levels fell, death rates went up.  The Honolulu Heart Program study had 8,000 participants and in their 2001 publication:

“Long-term persistence of low cholesterol concentration actually increases the risk of death. Thus, the earlier the patients start to have lower cholesterol concentrations, the greater the risk of death.”

Finally, there is the recent J-LIT study of the Japanese Lipid Intervention Trial.  This was a study of over 47,294 people over 6 years.  In table 6 on page 1092, is states that the cardiovascular mortality in the lowest cholesterol group (under 160 mg/dl) was over 6 TIMES (6.23x) the mortality rate of the "normal" cholesterol group (200-219 mg/dl). In other words, those with the lowest cholesterol had the highest death rate, and those with cholesterol levels that would today be called “dangerous” and put on a statin drug had the lowest death rate. 

I will end this section by quoting Malcolm Kendrick from 2005 on a different study: “The great ship Cholesterol-Lowering has ripped its guts out on the harsh rocks of evidence, but still it does not sink”

Statin Drugs

So as you can see above, lowering your cholesterol levels may actually increase your chance of dying. So with all this modern science and data showing that the Lipid Hypothesis is wrong in every way, why do doctors still believe in it and prescribe cholesterol lower drugs (statins)?  Well I think it is important to point out that doctors on average receive 23.9 hours of nutritional education in medical school! (source) That's right, with 4 years of pre-med, 4 years of medical school and 4 years of residency, the average doctors spends less than 24 hours getting nutritional education. This is a major problem in general but especially in this case because one of the primary factors in CAD is nutrition.  More on this in my next post.

I also think it is important to mention that statin drug pharmaceutical sales are over $35 Billion worldwide in 2011 (source). This is an industry force that isn't going away without a major fight. Not only that, but they are trying to expand their customer base.  Yes, the American Academy of Pediatrics recommended giving kids as young as 8 years old statins!!  (source)

Statin drugs should never be taken by women, as preventative or for post heart attack (source by Dr. Stephen Sinatra - audio).  Epidemiologist David Jacobs of the University of Minnesota, Twin Cities, brought together researchers from 19 studies around the world.  He reported to National Heart, Lung, and Blood Institute (NHLBI), which in 1990 hosted a conference to discuss the issue. When investigators tracked all deaths, instead of just heart disease deaths, the cholesterol curves were U-shaped for men and flat for women. In other words, men with cholesterol levels above 240 mg/dl tended to die prematurely from heart disease. But below 160 mg/dl, the men tended to die prematurely from cancer, respiratory and digestive diseases, and trauma. As for women, if anything, the higher their cholesterol, the longer they lived (source).

On top of all of this, the side effects of statins are numerous and serious. Statins are marvelous cholesterol killers because they intercept about 20 different biochemical pathways; one of those pathways is for CoQ10 and CoQ10 is one of the most important nutrients to protect your immune system. CoQ10 is also very good for heart health.  Isn't it ironic that this drug that is supposes to protect you from heart attacks severely damages one of your bodies biggest mechanisms for maintaining a health heart (CoQ10)?  I won't go into all the side effects (erectile dysfunction, muscle cramps, heart failure, cancer, loss of memory or lowered thinking ability, muscle pain or fatigue, neuropathy, etc) as there are many other sources for that information.

It is my belief that Statin drugs are one of the biggest hoaxes perpetrated on the public in history.

So what issues with cholesterol can be of concern?  There are four main causes of cholesterol problems, Stress, Smoking, Physical Inactivity and Poor Nutrition.  In our next post (located Here) we will talk about what really causes coronary artery disease and what we can do about it.

Posted by Maria Emmerich at 6:00 AM 28 comments

Meat Sauce

My Meat Sauce I Put On Everything

By juli, March 14, 2013, In 21DSD Entrees, Chicken, Pork, Recipe Box, Veggies

Home » 21DSD Entrees » My Meat Sauce I Put On Everything

Wearing high heels anywhere is so unrealistic. Especially while drinking. I’ve figured out, my toes almost always swell when I drink. Seriously, they get hot, swell up, and get tingly. Like when you’re on an airplane. Or pregnant. At least that’s what I’ve heard. I’ve never been with child.
I say this because I’m watching Sex and the City. But also, because I wore heeled boots out a week ago and my toes were crying after 2 or 7 shots of vodka. And when my toes cry, I whine. I’m an only child, so I’m sure you can imagine how often whining occurs. Answer: #fartoooften. I hate myself sometimes. And my toes. My chubby, drunk toes.
Speaking of drinking times, as you may know, the season finale of The Bachelor was on the other night and that meant girls night. And girls night includes food, more food, drinks, and more drinks. And gossip. It’s the best part. We decided for the finale, we would drink every time someone on the show said ‘connection’ or ‘love’. So I’m sure you can imagine how many drinks were downed. But that’s not what’s important here….
Sean chose….Catherine. WTF?!?! Are you serious? I was screaming at the TV. I’m not sure if it was the booze talking, but I was mad either way. This show is already complete bullsh*. I mean every single girl thinks she is in love with a guy after a couple weeks. And when I say a couple weeks, I am exaggerating. But then they make him pick the wrong person?! After telling us he’s a born again virgin?? Are you freaking serious? Way to make the Bachelor a COMPLETE bore. I mean come on. I was in pissed off-thrown for a loop-shock. It was so disappointing. I think he picked Catherine because he knew Lindsay would jump his bones. And he’s trying to keep it in his pants after living 28 years. I guess he made the right decision. Bastard.
I’m almost positive gluten poisoned me. Seriously. After eating gluten, then drinking a bottle of Kim Crawford, my stomach is f*cked. I am resisting to blame it on the alcohol. That would be out of my system by now. But this gluten from last week is haunting me. I’m pretty sure gluten is a parasite and this parasite is making babies in my insides that are very hungry children. Most are. And now they are drunk parasite children. What I’m trying to say here is, my insides hate me. I’m staying away from sugar, alcohol, and new restaurants. My life just got boring, didn’t it? Damnit.

5.0 from 6 reviews

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My Meat Sauce I Put On Everything

Prep time:  10 mins

Cook time:  20 mins

Total time:  30 mins

Serves: 2-4

Ingredients

• 1 pound ground chicken
• 1 pound bulk pork mild italian sausage
• 1 yellow bell pepper, diced
• 1 red bell pepper, diced
• 1 yellow onion, diced
• 2 (14 ounce ) cans of tomato sauce
• 3 garlic cloves, minced
• 1 teaspoon garlic powder
• 1 teaspoon cayenne pepper
• ½ teaspoon dried oregano
• ½ teaspoon dried parsley
• ½ teaspoon dried thyme
• ¼ teaspoon red pepper flakes
• ½ cup fresh basil, finely chopped
• salt and pepper, to taste
• 1-2 tablespoons fat of choice (I used bacon fat)

Instructions

1. Heat up a large saucepan over medium heat, add a couple tablespoons of fat of choice then add minced garlic cloves, the bell peppers and onion along with a little salt and pepper to the pan.
2. Move vegetables around until onions become translucent.
3. Add ground chicken and bulk italian sausage to the saucepan and break up the meat.
4. When meat has begun to cook through, add the spices.
5. When meat is almost done cooking, pour in the two cans of tomato sauce.
6. Salt and pepper once more, then reduce heat and let simmer for 5-7 minutes.
7. When all the flavors are well mixed, add the chopped fresh basil, mix well, and serve!
8. Easy peasy! Put on mushrooms, brussel sprouts, spaghetti squash, eggs, acorn squash, really anything you want. Or eat it cold. It’s pretty damn good cold.

 

How to Make Coconut Butter

from Jane's Healthy Kitchen

Coconut Butter

In: Ingredients

2

View all Jane’s recipes that use Coconut Butter
Raw coconut butter is one of my favorite foods! It is often called Creamed Coconut, or Coconut Cream. It is pure coconut meat that is ground into nut butter. This is a pure whole food, 100% Paleo, and so delicious it’s practically candy in the raw. Coconut Butter is not to be confused with coconut oil. My favorite brand is Artisana Coconut Butter. There are other good sources, such as Let’s Do Organic Creamed Coconut, Tropical Traditions, and Coconut Manna by Nutiva, all available in any whole foods grocery or online.
How to Make Homemade Coconut Butter
Coconut Butter can be expensive. You can save a lot of money by making it yourself. You need:
A high-speed blender, either a Blendtec or a Vitamix
2 to 7 cups of shredded unsweetened coconut flakes
1 glass jar
Fill your blender at least halfway with flakes (that’s a lot!) so it can stir properly. If your blender is small, start with 2 cups. If it is large, you can use up to 7 cups. It should be quite full. If your high-speed blender has a tamper tool, this may be useful.
Blend the coconut meat on high speed. The coconut will begin to break up. Have patience and keep going. After 30 seconds it will begin to liquefy. Slowly it will turn to butter. Blend until smooth and fine, at least a minute. Then pour the butter into a jar. This butter is highly condensed coconut meat. Just to give you an idea: 5 cups of shredded coconut will yield 2 cups coconut butter. It’s really delicious!
To use coconut butter
I use coconut butter in sauces, dressings, frostings, puddings and cheesecakes. You can soften it by putting the jar or container in a bowl of lukewarm water. This just takes a few minutes and makes it easier to measure. Coconut Butter is highly temperature sensitive. It softens to a thick liquid at 76 degrees F. At cooler temperatures it is solid, something like hard cheese. Click below to order.