Italian Food the Cureality Way


100% grain elimination is the theme that drives the Cureality nutrition approach. A common mistake made when eliminating grains is replacing wheat-based foods with gluten-free foods. Most gluten-free foods, as they are currently available in the supermarket, are made with rice starch, tapioca starch, cornstarch, and potato flour. These dried pulverized starches generate more insulin and blood sugar surges than wheat. Gluten-free foods made with these undesirable ingredients are free of the appetite stimulating gliadin protein and wheat germ agglutinin, a lectin protein unique to wheat that causes direct intestinal damage. However, at best they can be referred to as “less bad” or unwelcome additions to the diet. Increasing your intake of these junk carbohydrates is a recipe for weight gain, inflammation and sky high blood sugar.

When removing grains from the diet, the goal is to replace them with truly healthy alternatives that do not contribute to negative health consequences. There are several reasonable substitutions available that allow your favorite sauce and protein combos to shine in tasty pasta-like dishes. People following the Cureality nutrition approach frequently comment that they do not miss “real” pasta because of the available healthy replacements they have learned about and incorporated into their lifestyle.

Our nutritionist, Lisa G., is the champion at helping navigate this lifestyle. In this video, she demonstrates how to prepare spaghetti squash, which can be used to replace wheat-based pasta. In another video zucchini noodles are the star. Homemade meatballs, a zesty tomato sauce and zucchini “pasta” combine for a delicious meal. Who needs grains when you can enjoy meals that support increased energy and less joint pain? 


Loading
Is Lp(a) part of your legacy to your children?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Comments (21) -

  • craig&jan

    9/15/2009 4:59:09 AM |

    Finally switched to a new PCP who says she loves lipids!  Very interested in all facets of cardiac risk, thyroid, etc.

    My father is 88 and still very active. My mom passed away at 84 following her first health event which was a stroke.  
    I have been following this blog's recommendations for supplements, diet,etc. The new dr did a lipid panel and without any rx meds, my total was 199, HDL 61, Tri 68, LDL 124.  My Lp(a) was tested by my previous dr and was 34. I was told that was high and I probably had inherited my mother's pattern and she most likely had an Lp(a)problem. The new dr says I must go on Crestor 5mg a day to lower my LDL to 100. She says that will protect me from depositing more plaque in the coming years, in effect immobilizing the Lp(a). Would you say that was a fair assessment and reason to start on a statin?  She feels the lowest dose possible is enough to benefit by lowering the LDL.  Your post is exactly the situation I'm in and adding meds are my biggest question.  I will tell my children who are in their late 20's. I'm in my mid-50's with no other health issues.  I'd love your take on it.

    Thanks.

    Jan

  • craig&jan

    9/15/2009 4:59:09 AM |

    Finally switched to a new PCP who says she loves lipids!  Very interested in all facets of cardiac risk, thyroid, etc.

    My father is 88 and still very active. My mom passed away at 84 following her first health event which was a stroke.  
    I have been following this blog's recommendations for supplements, diet,etc. The new dr did a lipid panel and without any rx meds, my total was 199, HDL 61, Tri 68, LDL 124.  My Lp(a) was tested by my previous dr and was 34. I was told that was high and I probably had inherited my mother's pattern and she most likely had an Lp(a)problem. The new dr says I must go on Crestor 5mg a day to lower my LDL to 100. She says that will protect me from depositing more plaque in the coming years, in effect immobilizing the Lp(a). Would you say that was a fair assessment and reason to start on a statin?  She feels the lowest dose possible is enough to benefit by lowering the LDL.  Your post is exactly the situation I'm in and adding meds are my biggest question.  I will tell my children who are in their late 20's. I'm in my mid-50's with no other health issues.  I'd love your take on it.

    Thanks.

    Jan

  • Dr. William Davis

    9/15/2009 11:57:55 AM |

    Hi, Jan--

    Sadly, that is the typical primary care response, someone who has minimal to no insight into Lp(a).

    So, no, I would not agree with this approach that was first popularized by a single substudy performed by Dr. Greg Brown at the University of Washington.

    I take a very different view of Lp(a) that varies depending on age. However, this is a lengthy topic either for a future post or refer to the detailed discussions in the Track Your Plaque website.

  • ABick

    9/15/2009 3:47:10 PM |

    Dr. Davis - Is any amount of Lp(a) a significant risk factor for CVD?  Or is there a relatively safe threshold that if one is below there should be limited risk?

  • steve

    9/15/2009 4:42:52 PM |

    Dr Davis:  what would you say is a high Lp(a)? The NMR range is <75nmol, and the other measurement i think is <32or 40dl.  Would a 30-40 be high on NMR, or 15-20 per dl?
    Thanks,

  • Scott Miller

    9/15/2009 8:01:37 PM |

    Dr. Davis,

    I read all of your posts, greatly admire your practice, open-mindedness, and vast knowledge.

    I have measured my Lp(a) for several years, and have kept it at a bare minimum, usually below 8, most recent a reading of 3. I do this through a paleo-like diet:

    o High-fat (avoiding polyunsaturated fats, but high in saturated fats, mono unsaturated fats, and marine omega-3's)
    o Moderate protein (mostly from animal sources)
    o Low-carb (no grains, no added sugars, absolutely no processed fructose, and eating mostly high-water-volume vegetables, which are naturally very low in actual glucose polymers)

    My primary goals:
    o Maintain ultra low inflammation
    o Maintain low insulin usage (thru maintaining low-normal blood glucose, in the 80's)

    I'm 48, in supremely great health, and look around 35-yrs-old.

    My question: I've thoroughly looked for studies linking Lp(a) to gluten consumption, but I've come up empty. Are you aware of any studies?

  • Dr. William Davis

    9/15/2009 9:17:14 PM |

    AB and Steve--

    Because there are several different methods to measure Lp(a) for which the "reference ranges" differ, it is best to consult the range offered by the lab used, which are pretty good indicators of normal vs. abnormal.

    Scott--

    I know of no data specifically relating gluten to Lp(a). Anecdotally, there may be an effect, but it is likely relatively small.

  • Scott Miller

    9/16/2009 2:14:38 AM |

    Dr. Davis, I thought you had found in your practice a link between gluten and Lp(a). Or, at least, wheat and Lp(a)?

  • Dr. William Davis

    9/16/2009 2:30:01 AM |

    Hi, Scott-

    It's difficult to separate out the effects of wheat elimination vs. carbohydrate reduction, increased fat/oil intake. So I cannot say with absolute confidence that gluten specifically affects Lp(a).

    It's an interesting concept, but I don't believe that we have an answer.

  • David

    9/16/2009 4:41:08 AM |

    Dr. Davis- Have you ever seen Lp(a) cause heart disease in the very young? Under 35 or even under 30? I know that even children can have high Lp(a), and it makes me wonder if plaque growth is going on throughout childhood in these cases or if it is rather somehow "activated" once a certain point is reached and accelerates in a very short time toward the kind of events we see in the 40s and 50s age groups.

  • Lou

    9/16/2009 4:16:09 PM |

    Dr Davis

    I found a lab in Europe that will do an Lp(a) test and also Apolipoprotein A. I want to do the Lp(a) test as you suggest.

    The lab also offers an Apolipoprotein B test. Is the Apolipoprotein B of any use value? I couldn't see much info about it on your blog/book.

    Thanks
    Lou

  • Kent

    9/16/2009 4:54:47 PM |

    I see various thoughts and studies on the effects of monounsaturated fats on LP(a). I see Scotts example of using lots of saturated and monounsaturated fats and lowering his LP(a). I see other studies where they say monounsaturateds can raise LP(a) by 10-12%. What gives?

  • Dr. William Davis

    9/17/2009 1:45:11 AM |

    Hi, David--

    Rarely will Lp(a) cause heart disease before age 35. There are always exceptions, but they are exceptionally rare.


    Lou--

    Apo B is an improvement over calculated LDL. Yes, it is worth the few extra bucks. My personal favorite, however, is NMR LDL particle number, the best measure of LDl by a long stretch. Apo B is a second best.

  • Dr. B G

    9/17/2009 2:13:23 PM |

    Kent,

    Saturated fatty acids (SFA)indeed potently control Lp(a) in the clinical trials as well as anecdotally in our TYP membership. Why? SFA are actually hormonal in action, binders of receptors just like omega-3 fatty acids which lower inflammation and raise HDLs.

    There is a study that shows if Lp(a) is = or < than HDL2, Lp(a) is effectively 'neutralized'. Some of our members had HDL2 of > 40-50 mg/dl. In fact, Lp(a) and HDL track  together and  Dr. Davis' TYP program includes every facet and strategy that raises HDL to one's genetic potential:
    --thyroid and hormone replacement
    --wheat/gluten/carb elimination
    --vitamin D

    With every 10% increase in vit D, there is a ~1% increase in HDL. Did u know Crestor raises vit D by 159%?! Of course Crestor has NASTY side effects -- Crestor raises oxLDL + Lp(a)).

    -G

  • Dr. B G

    9/17/2009 2:13:23 PM |

    Kent,

    Saturated fatty acids (SFA)indeed potently control Lp(a) in the clinical trials as well as anecdotally in our TYP membership. Why? SFA are actually hormonal in action, binders of receptors just like omega-3 fatty acids which lower inflammation and raise HDLs.

    There is a study that shows if Lp(a) is = or < than HDL2, Lp(a) is effectively 'neutralized'. Some of our members had HDL2 of > 40-50 mg/dl. In fact, Lp(a) and HDL track  together and  Dr. Davis' TYP program includes every facet and strategy that raises HDL to one's genetic potential:
    --thyroid and hormone replacement
    --wheat/gluten/carb elimination
    --vitamin D

    With every 10% increase in vit D, there is a ~1% increase in HDL. Did u know Crestor raises vit D by 159%?! Of course Crestor has NASTY side effects -- Crestor raises oxLDL + Lp(a)).

    -G

  • Anonymous

    9/17/2009 6:32:59 PM |

    My brother had a MI right after he turned 29. My parents now in sixties, do not have cholesterol related heart disease yet although my mom has some issues now due to thyroid problems. She has also developed diabetes unfortunately.

    Would this be Lp(a) related incidence?

  • Kent

    9/18/2009 5:10:58 PM |

    Dr. BG, Thanks for your response on the subject of fats. I was aware that saturated fats could substatially lower LP(a), however my area of concern has more to do with the mono unsaturated fats. Scott mentioned how he had lowered his LP(a) with a diet that included high intake of the mono unsaturated fats. Yet, I have read elsewhere that the mono unsaturated fats can raise LP(a) by 10-12%. (Vessby B et al 2002).
    So I guess my question remains do monos raise or lower LP(a)

  • Florida Butterfly

    2/9/2010 2:07:29 AM |

    I am 22 and just found out that I inherited the elevated lp(a) levels. As of now my number his higher than my dads! He just avoided a heart attack, and had stents put in just before it reached that point. Needless to say I inherited it from him.  I am starting Niacin, only 100 mg.  I will say that it is a serious struggle for me to change my lifestyle as in diet and exercise so early.   My lp(a) # was 65

  • buy jeans

    11/4/2010 5:13:10 PM |

    (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

  • Anthony Cozzi

    11/24/2011 1:46:27 AM |

    Dear Dr. Davis
    I am 58 years old and have had three stents ( one in 2000 and two in 2008 ).  My Lp(a) is >200 according to my last Berkely Test in 2010.  I am soon having another Berkely Test and would like to know exactly what I should have tested besides my Lp(a) and particle size.  I have been taking Niaspan (1500mg daily) and Simcor 1000/20, Fish Oil and Vitamin D3 ( 6000 iu ) all daily.  Would you suggest me taking any DHEA ?  I would really appreciate hearing from you.  I live in Chicago and could visit your office. 708-925-3010.  Thank you.
    Anthony Cozzi

  • Dr. William Davis

    11/25/2011 2:12:20 PM |

    Hi, Anthony--

    Thyroid assessment is crucial in Lp(a): TSH, free T3, free T4. Also, a DHEA level. Both issues are very important.

    Sorry, but my practice is now closed to new patients, since we were booking 6 months in advance. However, much of this can be found in the Track Your Plaque website.

Loading